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27.2% of hepatocellular carcinomas showed p53 alteration ,but only 1 of the tumors with p53 alteration was well differentiated. 27.2% of hepatocellular carcinomas showed p53 alteration ,but only 1 of the tumors with p53 alteration was well differentiated. : Alterations in p53 are a common event in advanced epithelial ovarian cancer. A mutation in p53, but not overexpression of p53, is associated with a short-term survival benefit. A HLA-A2 restricted human CTL line recognizes a novel tumor cell expressed p53 epitope. A case-control study showed that polymorphism in codon 72 of the p53 gene was not a cervico-uterine cancer risk factor in Mexico. A cytoplasmic accumulation of wild-type p53 in human primary glioblastomas correlates with GFAP and vimentin expression. Cytoplasmic p53 is inactive in growth suppression. A link between the p53 germ line polymorphisms and white blood cells apoptosis in lung cancer patients. A loss of wild-type p53 gene function and consequent p53 overexpression in gastric carcinomas may be involved in early stages of tumor progression. A lower invasiveness and shorter survival was seen in tumors with a TP53 mutation. A new germline p53 mutation was found associated with a choroid plexus papilloma. The 7-BP insertion in exon 5 causes a frameshift from 161-182 and affected transactivation but not apoptosis induction. A novel germline mutation in p53 gene was found in a patient with Li-Fraumeni syndrome. A point mutation of p53 in a lung cancer patient simultaneously can elicit not only a humoral immune response against overexpressed p53 protein, but also a specific cytotoxic T lymphocyte response against the mutated epitope of p53 in the same patient. A potential association of P53 codon polymorphism was found with increased susceptibility to gastric cancer. A proteasome inhibitor, lactacystin, enhances TNFalpha cytotoxicity in p53-positive and -negative cells. A selective growth advantage for cells carrying a type of TP53 mutation seen in breast carcinomas when the mutation resides on Arg72 allele. These are not seen in colorectal neoplasms. A senescence rescue screen identifies BCL6 as an inhibitor of anti-proliferative p19(ARF)-p53 signaling. A shift from one p53 intron 2 genotype in the blood to another genotype in the tissue may be a prognostic factor in ovarian cancer patients. A significant association between p53 gene Bam HI RFLP polymorphism and the infarction volume was found in patients with carotid atherothrombotic stroke from Moscow population. A significant correlation between YB-1 and PCNA-LI was found, but none was found between p53 expression and PCNA in lung cancer. A significant increase in p21, p53, and fas mRNA expression were reported in the proximal incompetent veins. The expression of p21 correlated with expression of p53. Fas overexpression did not correlate with p53 expression. A spontaneous increase of wild-type p53 occurring in ageing normal human MRC-5 fibroblasts is associated with irreversible reduction of proliferative potential. A two-stage, p16(INK4A)- and p53-dependent keratinocyte senescence mechanism that limits replicative potential independent of telomere status. ARF may regulate p53 acetylation and stability in part by inhibiting tripartite motif-containing 28-MDM2 binding. ASPP2/(53BP2L) protein levels by proteasomal degradation modulates p53 apoptotic function. ATR-p53 pathway is suppressed in noncycling lymphocytes via ATR downregulation. Aberrant HPLC chromatographies were found in tumor tissues, while their normal-adjacent counterparts running in parallel showed a normal shape. Abnormality of the p53 pathway was detected in cervix cancer and in CINs. Acetylation of p53 in vivo may contribute, at least in part, to its transcriptional activation functions. Activated caspase-8 initiates the release of cytochrome c during thymoquine-induced apoptosis, thus offering a potential mechanism for TQ-induced apoptosis in p53-null HL-60 cancer cells. Activated p53 suppresses EZH2 expression, suggesting a further role for p53 in epigenetic regulation and in the maintenance of genetic stability. Activation domain 2 of p53 is required for induction of the proapoptotic target gene insulin-like growth factor binding protein 3 (IGFBP3) and p53 basic domain inhibits induction of this gene. Activation of p53 reduces binding and relieves transcriptional repression of the Dnmt1gene, whereas loss of p53, a frequent, early event in tumorigenesis, may significantly contribute to aberrant genomic methylation. Activities of p53 are regulated during the cell cycle by E2F/p53 interactions; phosphorylation of p53 at Ser315 is required for this regulation. Adenovirus encoding HIV-1 Vpr activates caspase 9 and induces apoptotic cell death in both p53 positive and negative human tumor cell lines. Adenovirus infection does not need direct binding of E1B-55-kDa with p53 to inactivate p53, and forced p53 activity with consecutive apoptosis does not severely impair virus replication. Adenovirus-p53 induces the expression of a variety of proapoptotic genes and that lack of induction in one of these genes does not block Ad/p53-mediated cell killing in human lung cancer cells. Affects relative biological effectiveness of light ions in human tumoural cell lines. Akt enhances Mdm2-mediated ubiquitination and degradation of p53. Alterations of the TP53 gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome. Among women with p53 alterations, adjuvant radiotherapy substantially increased survival. An identical single nucleotide deletion within the C/EBP-like site of the promoter in 2 OF 18 Li-Fraumeni families. This site is not utilized in the wild type TP53 promoter and mutation of this site in LFS/LFL does not have a functional effect. Analysis of BRCA1, TP53, and TSG101 germline mutations in German breast and/or ovarian cancer families. Analysis of expression levels of p21(waf1), as well as the activity of caspase-3 and caspase-8, allowed us to characterize some aspects of the arrest of PC-3 cells in G2 and the apoptotic response to oxidative stress in the absence of functional p53. Anoxia induces macrophage inhibitory cytokine-1 (MIC-1) in glioblastoma cells independently of p53 and HIF-1.The macrophage inhibitory cytokine-1 (MIC-1) gene was identified as a most prominent p53 target gene upon gene expression profiling. Anwuploidy of chromosomes 7, 8, 9, and 17 and of TP53 gene deletion and overexpression in intestinal mettaplasi samples from cancer-free patients. Apoptotic index (includes nick-end labeling) and bcl-2 do not correlate with key clinical data (prognosis and blood counts at diagnosis) in patients with myelodysplastic syndrome, while p53 protein levels do. Association association between lack of response to 5-fluorouracil and mitomycin and mutations affecting the L2/L3 domains of the p53 protein. Asymmetric self-renewal and immortal DNA strand cosegregation are regulated by the p53 cancer gene. Atypical meningioma showed TP53 mutations and a 22q loss of heterozygosity (LOH), while glioblastoma showed epidermal growth factor receptor (EGFR) amplification and TP53 mutations. BRCA1-BARD1 complexes act as an adaptor to mediate phosphorylation of p53, influencing G(1)/S cell cycle progression after DNA damage. Bcl-2 constitutively suppresses aptoptosis dependent on this protein in colorectal cancer cells. Binding to the p53 binding sites of the Mdm2 promoter alleviates the requirement for p53 C-terminal activation. Both p53 and c-erbB-2 proteins appear to be involved at an early stage of malignization of pleomorphic adenoma. Both survivors and nonsurvivors of fluorouracil treated rectal neoplasms show high P53 expression. Bulgarian patients with invasive breast cancer screned for p53 gene mutations registered a 33.33% frequency of mutations. By inhibiting p21(Cip1) expression Myc favours the initiation of apoptosis, thereby influencing the outcome of a p53 response in favour of cell death. C-terminus of p53 is required for G(2) arrest. CARF is co-regulated with ARF and cooperates with it in activating p53. CD27 and CD40 co-stimulatory signals regulated the p53-amplified apoptotic pathway in B cells through the inhibition of p53-independent apoptotic pathway primarily induced by BCR ligation. CHIP-induced degradation was observed for mutant and wild-type p53, which transiently associate with molecular chaperones Hsc70 and Hsp90 and can be diverted onto a degradation pathway through this association. COX-2-positive prostate cancer cells can have impaired p53 function even in the presence of wild-type p53 and that p53 activity can be restored in these cells via inhibition of COX-2 activity. CP-31398-mediated stabilization of p53 may result from reduced ubiquitination, leading to high levels of transcriptionally active p53. Ca2+ binding of human p53 tumor suppressor target peptide (residues 367-388) to rat S100B decreases the Ca2+ dissociation rate by approximately an order of magnitude. Caffeine induces cell cycle arrest and apoptosis in association with activation of p53 by a novel pathway to phosphorylate the Ser-15 residue and induction of phosphorylation of cdc 2 in leukemic cells with normal p53. Cancerous hyper-mutagenesis in p53 genes is possibly associated with transcriptional bypass of DNA lesions. Cellular effects of CPT-11 on colon carcinoma cells: dependence on p53 and hMLH1 status. Ceramide may function as a mediator of p53-independent apoptosis in human glioma cells. ChIP assays have shown that following radiation treatment the p21 and puma promoters, but not bax, have increased p53 binding. The presence of constitutive binding to putative p53 DNA binding sites in other genes was determined. Changes of NF-kB, p53, Bcl-2 and caspase in apoptosis induced by JTE-522 in human gastric adenocarcinoma cell line AGS cells: role of reactive oxygen species. Characterization of the p53-rescue drug CP-31398 in vitro and in living cells. Clear need in human melanoma cell lines to disrupt both RB and p53 pathways and recurrent mechanisms which play into the unique genetic vulnerabilities of this tumor type. Clinical course of B-CLL in group of patient with trisomy 12, trisomy 12 and TP53 deletion simultaneously is more aggressive compared to the course of disease of patients with no cytogenetic aberrations. Cloning and characterization of a novel gene PDRG that is differentially regulated by p53 and ultraviolet radiation. Co-mutation of p53 and K-ras gene has neither synergic carcinogenesis-promoting effect, nor prognostic effect on rectal cancer. Codon 249 mutation in exon 7 of this gene in plasma DNA may be a new early diagnostic marker of hepatocellular carcinoma in Qidong risk area, China. Codon 72 of P53 genes may represent a risk factor for developing ovarian or endometrial neoplasms. Coexpression of P-glycoprotein, Ets-1, and p53 in oral carcinoma is associated with poor prognosis. Colorectal cancers not expressing hMLH1 or hMSH2 may have distinct features from those expressing these mismatch repair proteins. p53 expression appears to be implicated in a compensatory pathway with mismatch repair proteins. Comparative study in the expression of p53, EGFR, TGF-alpha, and cyclin D1 in verrucous carcinoma, verrucous hyperplasia, and squamous cell carcinoma of head and neck region. Comprehensive site-directed mutagenesis technique & a yeast-based functional assay were used to construct, express, & evaluate 2,314 p53 mutants representing all possible AA substitutions caused by a point mutation throughout the protein. Constitutive dephosphorylation at Ser 376 correlated with the nuclear accumulation of p53, but not with the transcriptional activity of the protein in glioma. Cooperation of two mutant p53 alleles contributes to Fas resistance of prostate carcinoma cells. Copper alters the conformation and transcriptional activity of TP53 in Hep G2 cells. Correlates with invasiveness including vascular permeation, grade of cellular differentiation, incomplete capsule and multinodular lesions. More recurrence. May also influence disease recurrence interval and survival time. Correlation between p53 accumulation and survival in bilharziasis associated bladder squamous cell carcinoma. Crucial role of p53 C-terminal phosphorylation in the regulation of its DNA-binding activity. Curcumin induces apoptosis in human breast cancer cells through p53-dependent Bax induction. Cyclin A1 methylation was inversely related to p53 mutational status in primary tumors, and forced expression of cyclin A1 resulted in robust induction of wild-type p53 in HNSCC cell lines. Cyclin D1, p53, and p21Waf1/Cip1 have roles in progression of serous epithelial ovarian cancer. Cyclooxygexnase-2 in p53 wild-type cancer cells does not affect the cytoplasmic or nuclear levels of p53. Cyr61 activated the beta-catenin/TCF4 complex, which promoted the expression of c-myc and the latter induced expression of p53. DN-p73 is activated after DNA damage in a p53-dependent manner to regulate p53-induced cell cycle arrest. DNA repair of the gene region in two human bladder carcinoma cell lines. DNA-PK and p53 may form a sensor complex that detects the disruption of DNA replication caused by nucleoside analogue incorporation and may subsequently signal for apoptosis. DNA-damaging stresses showed a strong p53-dependent element in their responses, no discernible p53-dependent responses were triggered by the non-DNA-damaging stresses. DNMT1- and p53-mediated methylation of the survivin promoter, suggesting cooperation between p53 and DNMT1 in gene silencing. Data describe the correlation between inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 activities and p53 gene status in head and neck squamous cell carcinomas in vivo and in vitro. Data may provide evidence to support the idea that p53 expression is related to multidrug resistance (MDR) in combination of 5-fluorouracil plus cisplatin therapy of gastric cancer cell lines. Data reveal that controlled MDM2 degradation is an important new step in p53 regulation. Data show that 5-lipoxygenase activity increases during senescence-like growth arrest via a p53/p21-dependent pathway in both human and mouse embryo fibroblasts. Data show that Topors enhances the conjugation of the small ubiquitin-like modifier 1 (SUMO-1) to p53 in vivo and in a reconstituted in vitro system. Data show that activated protein C directly prevents apoptosis in hypoxic human brain endothelium through transcriptionally dependent inhibition of tumor suppressor protein p53. Data show that aspirin decreases endothelial cell proliferation through cell cycle arrest mediated by enhanced p53 expression. Data show that growth arrested keratinocytes may resist ultraviolet-light induced apoptosis by inactivating the pro-apoptotic function of p53. Data show that human papillomavirus E6 oncoprotein does not prevent p53 or p300 recruitment to the chromatin but inhibits p300-mediated acetylation on p53 and nucleosomal core histones. Data show that latent infection with Kaposi sarcoma-associated herpesvirus in B lymphocytes can be terminated by glycyrrhizic acid. Data show that squamous cell carcinoma cells escape suspension-induced, p53-mediated anoikis by forming multicellular aggregates that use fibronectin survival signals mediated by integrin alpha(v) and focal adhesion kinase. Data show that the 249(Ser) p53 mutation in plasma is strongly associated with hepatocellular carcinoma (HCC). Data show that the fundamental active unit of p53 appears to be the tetramer, which is induced by DNA binding. Data show that the status of codon 72 polymorphism and p53 mutations can be used as a means for prediction of treatment response, although variables for each cancer type requires detailed evaluation. Data show that, when overexpressed, ribosomal protein L23 inhibits HDM2-induced p53 polyubiquitination and degradation and causes a p53-dependent cell cycle arrest. Data showed that disabling of the p53 pathway was frequent event in oral carcinoma. Data suggest a model in which p53 directly recruits a TRRAP/acetyltransferase complex to the mdm2 gene to activate transcription. In addition, this study defines a novel mechanism utilized by the p53 tumor suppressor to regulate gene expression. Data suggest that MTBP differentially regulates the activity of MDM2 towards two of its most critical targets (itself and p53) and in doing so significantly contributes to MDM2-dependent p53 homeostasis in unstressed cells. Data suggest that both before and after UV irradiation, DDB2 directly regulates p53 levels, while DDB2 expression is itself regulated by p53. Data suggest that certain p53 mutations may have prognostic value in superficial bladder transitional cell carcinoma, even though they were not associated with other classic recurrence and tumor progression parameters. Data suggest that geminin is required for suppressing overreplication in cells with wild-type or mutant p53 and that a G(2)/M checkpoint restricts the proliferation of cells with overreplicated DNA. Data suggest that naturally occurring genetic variability at p53 gene explains part of the inter-individual difference in the in vitro susceptibility to a chemotherapeutic drug. Data suggest that securin is a p53 target gene and may play a role in p53-mediated cellular response to DNA damage. Daxx significantly augmented p53-mediated transcription and the Adenovirus E1B 55-kDa protein eliminated this effect. Decreased level of the phosphorylation is associated with basal cell carcinomas of skin. Defect of spindle checkpoint gene Mad2 and mutation of p53 gene are involved mainly in colorectal carcinogenesis, and cancer/normal tissue ratio >2 is associated with prognosis of colorectal cancer. Dehydroepiandrosterone increased the expression of p53 and p21 mRNAs. Delayed activation of p53 occurrs in the progeny of irradiated cells. DeltaN-p63-alpha mediates the silencing of its own promoter thereby altering the pattern of p53-target gene expression. DeltaNp73alpha not only acts as an inhibitor of p53/TAp73 functions in neuroblastoma tumors, but also cooperates with wt-p53 in playing a physiological role through the activation of BTG2TIS21/PC3 gene expression. Deregulated c-Myc partially disabled the p53-mediated DNA damage response. Detection of P53 may be used as the screening marker for diagnosis of polycyclic aromatic hydrocarbons (PAHs)-related lung cancer related lung cancer, and may supplement the diagnostic value of conventional cytology. Deubiquitination of p53 by HAUSP is an important pathway for p53 stabilization. Differential expression of genes induced by resveratrol in LNCaP cells: P53-mediated molecular targets. Differentiating human keratinocytes are deficient in p53 but they preserve global nucleotide excision repair as well as expression of genes encoding key DNA damage recognition proteins. Disruption of p53-p21/WAF1 cell cycle pathways contributes to tumor progression and worse clinical outcome of hepataocellular hepatoma. Down-regulation of Cdc7 by small interfering RNA in a variety of tumor cell lines causes an abortive S phase, leading to cell death by either p53-independent apoptosis or aberrant mitosis. Downregulation of p16(INK4a) and loss of wild-type p53 expression occurs after escape from cell immortalization. During apoptosis, p53 activates transcription of PAC1 by binding to a palindromic site in the PAC1 promoter. E1B-55K-anchored proteome is linked to polyubiquitination of p53 in vitro. E4orf6 uniquely utilizes two BC-box motifs for degradation of p53 and another target, Mre11. Effect of hibuscus polyphenol extracs in human gastric carcinoma cells is mediated via p53 signaling and p38 MAPK/FasL cascade pathway. Efficient repair of bulky anti-BPDE DNA adducts from non-transcribed DNA strand requires functional p53 but not p21(waf1/cip1) and pRb. Emerging evidence in this review discusses a key survival/death checkpoint in both peripheral and central neurons that involves the p53 tumor suppressor and its newly discovered family members, p73 and p63. Epigallocatechin-3-gallate increased expression of tumor suppressor protein p53 in brest cancer cells. Epigallocatechin-3-gallate-induced stabilization of p53 caused an upregulation in its transcriptional activity, thereby resulting in activation of its downstream targets p21/WAF1 and Bax. Evaluation of HIF-1alpha, p53 and p21 protein expression is a very useful and powerful indicator of sensitivity to chemotherapy and radiation resistasnce in human esophageal cancer. Evaluation of relationship between chromosome 22 and p53 gene alterations and the subtype of meningiomas by the interphase-FISH technique. Excision of nucleoside analogs from DNA by p53 protein suggests a potential cellular mechanism of resistance to inhibitors of human immunodeficiency virus type 1 reverse transcriptase. Expression of Id helix-loop-helix proteins in colorectal adenocarcinoma correlates with p53 expression and mitotic index. Expression of apoptosis-inductive genes were increased by X-ray irradiation in squamous cell carcinoma cells(SAS) with wild-type p53, but not in SAS cells expressing mutated p53. Radiation sensitivity may come from expression of apoptosis-related genes. Expression of mitotic spindle checkpoint protein hsMAD1 correlates with cellular proliferation and is activated by a gain-of-function p53 mutant. Expression of p53 and bcl-2 proteins in acute leukemias: an immunocytochemical study. Expression of p53 in primary central nervous system diffuse large B-cell lymphoma may be a prognostic marker for poor overall survival. Expression of p53 in renal carcinoma cells is independent of VHL. Expression of p53 is associated with NIH risk category, various pathological features, and clinical outcome, and may be independently prognostic for gastrointestinal stromal tumours. Expression of p53 protein can enhance proliferation of HCC cells and suppress apoptosis of HCC cells after transcatheter arterial chemoembolization. Expression of p53R2, newly p53 target in oral normal epithelium, epithelial dysplasia and squamous cell carcinoma. Expression of this apoptosis-related protein may be a useful marker in cervix cancer development. Expression of this molecule and its correlation with prognostic markers in patients with head and neck tumors. Expression or this protein does not predict outcome in colorectal cancer patients. FADD/caspase-8 pathway induces apoptosis through p53 in human pre-malignant and malignant cells. FAK and Akt are activated in the attached fibroblast-populated collagen matrix whereas the p53 level is relatively low; matrix detachment downregulates FAK and Akt activity and induces p53. FAK can suppress p53-mediated apoptosis and inhibit transcriptional activity of p53. FGFR3 and Tp53 mutations do not appear to be associated with progression of T1G3 transitional bladder carcinomas. Fas-mediated apoptosis is dependent on wild-type p53 status in human cancer cells expressing a temperature-sensitive p53 mutant alanine-143. Fibrillar aggregates of the p53 core domain contribute to the loss of function of p53 and seed the accumulation of conformationally altered protein in some cancerous cells. Functional mutants of the sequence-specific transcription factor p53 and implications for master genes of diversity. GSH plays a vital role in the protection of tri- and perchloroethylene-induced oxidative stress & apoptosis, which may be mediated through a p53-dependent pathway. GSK3-dependent phosphorylation of Mdm2 regulates p53 abundance. Gene-profiling experiments of breast cancer cells infected with wt p53 revealed both MASPIN and desmocollin 3 (DSC3) to be p53-target genes, even though both genes are silenced in association with aberrant cytosine methylation of their promoters. Genetic alterations of INK4alpha/ARF locus and p53 are observed in human hepatocellular carcinoma. Genetic mutation analysis was performed and revealed a germline p53 mutation of CGT > CAT at codon 273. Genetic signature of oligoastrocytomas correlates with tumor location and denotes distinct molecular subsets. Genetic status of cell cycle regulators in squamous cell carcinoma of the oesophagus: the CDKN2A (p16(INK4a) and p14(ARF) ) and p53 genes are major targets for inactivation. Germline mutations of this protein exist in a cohort with childhood sarcoma: sex differences in cancer risk. GgA transition in codon 175 of the p53 gene as a potential marker of colon cancer progression. Glioma cells with functional p53 were relatively resistant to gamma-radiation, and ceramide may play an important role in caspase activation during gamma-radiation-induced apoptosis of glioma cells lacking functional p53. H pylori affect the p53 pattern in gastric mucosa when microsatellite system fails to work. HHV-6 has a mechanism for retaining p53 within the cytoplasm and protects the infected cells from apoptosis. HIPK2-mediated enhancement of p53-dependent transcription, p53 serine 46 phosphorylation and the antiproliferative function of HIPK2 strictly rely on the presence of PML. HSU94788 may not be the wild-type p53 sequence. AF136270 and AF135120 may be the correct wild-type intron 7 sequences. Ha-Ras(G12V) induced senescence regardless of p53 status and telomerase activation. Haplotype analysis also showed a significant association between TP53 and schizophrenia. These results provide further evidence that TP53 may play a role in the pathogenesis of schizophrenia. Haplotype structure of TP53 locus in Indian population and possible association with head and neck cancer. Hepacivirus core protein modulates p53 transcription regulatory activity and post-translational modification. Hepatitis B virus X protein in liver cells down-regulates the expression of PTEN and activates AKT and affects p53-mediated transcription of PTEN. Here we showed that 361 out of 1501 p53 responsive genes contained p53 consensus DNA-binding sequence(s) in their regulatory region, approximately 80% of which were repressed by p53. High p53 protein level is associated with advanced TNM stage and positive nodal status of squamous cell carcinoma of hypopharyngeal cancer. Histone deacetylase inhibitors can induce Gadd45 through its promoter without the need for functional p53, and Oct-1 and NF-Y concertedly participate in Trichostatin A-induced activation of the gadd45 promoter. Homozygosity for Pro of p53 Arg72Pro is potentially one of the genetic risk factors for hepatocarcinoma in a Chinese population. Hsp90 chaperone activity is important for the transcriptional activity of genotypically wild-type p53. Hsp90 is required to maintain the folded, active state of p53 by a reversible interaction. Hsp90-binding immunophilins link p53 to dynein during p53 transport to the nucleus. Human p14(ARF)-mediated cell cycle arrest strictly depends on intact p53 signaling pathways. Human papillomavirus infection and/or changes in p53 protein coexist in oral cavity papillomas. Human tumor suppressor ARF impedes S-phase progression independent of p53. Human wild-type p53 inhibits homologous recombination between substrates for conservative HR & for gene deletions. Non-homologus end-joining was downregulated after p53 expression. p53 mutations at codon 281, 273, 248, 175, or 143 disrupted DSB repair. Hypophosphorylation of Mdm2 augments p53 stability. ING1 expression is frequently associated with Adenocarcinoma of the esophagogastric junction tumorigenesis, further supporting its role as a tumor suppressor gene, and ING1 expression is independent of p53 status. ING1 has a subtle antiproliferative effect even in the absence of p53, and ING1b enhances the DNA damage responses through p53-dependent and -independent mechanisms. IRF-1 and the tumour suppressor protein p53 are coordinately up-regulated during the response to DNA damage in an ATM-dependent manner. IRF-1-p300 interface as an allosteric modifier of DNA-dependent acetylation of p53 at the p21 promoter. Identification of a novel mouse gene, mRTVP-1, as a p53 target gene. The mRTVP-1 protein has 255 amino acids and differs from the human RTVP-1 protein by two short in-frame deletions of two and nine amino acids. (mRTVP-1). IkappaBalpha x p53 complex plays an important role in responses involving growth regulation, apoptosis, and hypoxic stress. Immunohistochemical expression of this protein in squamous cell carcinomas from immunosuppressed renal transplant recipients and immunocompetent individuals. Immunostaining of p53 accumulation in families with multiple glioma pts showed that p53 alterations are as common in familial as in sporadic gliomas.Germline p53 mutations in exons 4-10 were not found. In adenocarcinomas, no statistically significant correlation was found between K-ras mutational status and p21WAF1/CIP1 and p53 expression. In carcinoma in situ tumors, p53 expression is not associated with clinical outcome. In human osteosarcomas, hypermethylation of HIC1 is frequent only in tumors with p53 mutation. In operable non-small lung cell cancers, there may be different relationship of this protein with paatient outcome. In response to irradiation, the amount of p53 protein synthesized in patients with AT and NBS was significantly lower than that in normal cells. Inactivation of p21WAF1 sensitizes cells to apoptosis via an increase of both p14ARF and this protein and an alteration of the Bax/Bcl-2 ratio. Individuals carrying Arg allele compared to those with Pro allele have an increased risk for esophageal squamous cell carcinoma. Induction of gene amplification is a gain-of-function phenotype of mutant p53 proteins. Inhibition of COX-2 in colon cancer cell lines by celecoxib increases the nuclear localization of active p53. Inhibition of p53 causes ubiquitination and down-regulation, through increased degradation, of the IGF-1R in human malignant melanoma cells. By sequestering Mdm2 in the cell nuclei, the level of p53 may indirectly influence the expression of IGF-1R. Integrin alphav controls melanoma cell survival in 3D-collagen through a pathway involving p53 regulation of MEK1 signaling. Interaction between bcl-2 and P53 in neoplastic progression of basal cell carcinoma of the head and neck. Interaction with Brn-3a in sensory neurons may be critical for modulating p53-mediated gene expression and hence cell fate. Interactions between p53, hMSH2-hMSH6 and HMG I(Y) on Holliday junctions and bulged bases. Interacts with WT1 in insulin-like growth factor-I receptor gene regulation. Interferon alpha-induced promyelocytic leukemia protein was unable to recruit p53 into nuclear bodies and its downregulation by RNA, Small Interfering did not alter CD95 expression. Involvement of TP53 in apoptosis induced in human lymphoblastoid cells by fast neutrons. Irinotecan resistant colorectal cancer lines are resistanst both in the presence or absence of p53. L11 functions as a negative regulator of HDM2 and there might exist in vivo an L11-HDM2-p53 pathway for monitoring ribosomal integrity. LC8 binds to p53-binding protein 1 and mediates DNA damage-induced p53 nuclear accumulation. Ligase dead mutants of Mdm2 did not act in a dominant negative manner to reactivate p53 and they are not oncogenes in human mammary epithelial cells. Limited activation of the PCNA promoter by p53 and its modified forms would restrict the amount of PCNA made available for DNA repair. Loss of heterozygosity at TP53.A (p53 gene exon 2-3) in 4 of 20(20%), at TP53.B (p53 gene exon 4) in 6 of 20(30%), and at TP53.G (p53 gene exon 11) in 0 of 20(0%) in hepatocellular carcinoma. Loss of p21 and/or p53 might not predict for prognosis in oropharnyggeal squamous cell carcinoma. Loss of p53 function leads to myeloma cell progression and resistant phenotype through bcl-2-related mechanisms. Loss of p53, directly or indirectly, perturbs the normal regulation of phosphorylation of serine 10 in histone H3. Loss or inactivation of p33(ING1b) normal function may be an important mechanism for the development of hepatocellular carcinoma retaining wild-type p53. Low p53 expression attenuates HIF-1 transactivation by competing for p300. High p53 expression destroys the HIF-1alpha protein.Once p53 becomes activated under conditions of severe hypoxia/anoxia, it contributes to terminating HIF-1 responses. Low-dose 5-aza-2'-deoxycytidine (DAC) induced enhancement of apoptosis mediated by Adenovirus-p53 infection, and ectopic overexpression of procaspase-9. Lung-specific expression of human point mutant p53-273H (under the SP-C promoter) is associated with a high frequency of lung adenocarcinoma in transgenic mice. This mutation is frequent in human lung tumors. MDMX post-translational processing may be regulated by p53. MDMX, when exceedingly overexpressed, inhibits MDM2-mediated p53 degradation by competing with MDM2 for p53 binding. MDMX-mediated regulation of p53 activity during development. MDR functional phenotype could be associated with p53 mutation in the advanced stage of leukemias. MNNG induces apoptosis in lymphoblastoid cells by activating the p53-dependent Fas receptor-driven pathway. MUC1 regulates p53-responsive genes and thereby cell fate in the genotoxic stress response. MYCL1, FHIT, SPARC, p16(INK4) and TP53 genes associated to lung cancer in idiopathic pulmoary fibrosis. Many genes are affected by TP53 gene dosage for their expression. We report several candidate genes as potential downstream targets of p53 in nonstressed cells. Among them, CSPG2 is validated as being directly transactivated by p53. Many p53-defective tumors retain activity of the apoptosome, which is therefore a potential target for cancer chemotherapy. Inhibition of ACS may be a novel strategy to induce the death of p53-defective tumor cells. Mdm2 and mdmx prevent ASPP1 and ASPP2 from stimulating the apoptotic function of p53 by binding and inhibiting the transcriptional activity of p53. Mdm2-mediated p53 ubiquitination is suppressed by HIF-1 alpha, which blocks Mdm2-mediated nuclear export of p53. Methylation of CpG and CCWGG motifs in the promoter of TP53 could represent a novel mechanism leading to functional impairment of this tumor suppressor gene in ALL. Modified DNA is recognized by ""latent"" and ""active"" protein p53. Mutant p53 can delay growth arrest in senescing fibroblasts without reducing p21(WAF1) expression. Mutated in choroid plexus carcinoma. Mutated-p53 (Asp281His), in head & neck cancer cells prevents cell death from DNA damage. This probably accumulates genetic alterations and accelerates the malignant progression of the cells by DNA damaging therapy. Mutation of human thioredoxin reductase 1 promotes p53-dependent gene expression. Mutation of p53 gene endows gliomas with an angiogenic phenotype by reducing thrombospondin-1 production as well as enhancing the angiogenesis inducers in the early phase of malignant progression. Mutation of p53 is significantly associated with gain of 20q, 13q, and 8q and loss of 18q in colorectal adenocarcinoma. Mutation pattern included base substitution (point mutation, G-->T, T-->G) and frame-shift mutation (base insertion and base loss). Mutations for basal cell carcinoma (BCC), were screened in 15 cases of sporadic BCCs that developed in sun-exposed skin region in a Korean population. Mutations in APC, Kirsten-ras, and p53--alternative genetic pathways to colorectal cancer. The most common combination of mutations was p53 and APC (27.1%), whereas mutations in both p53 and K-ras were extremely rare. Mutations in PTEN/MMAC1 gene correlated inversely with an altered p53 status. Mutations in exons 4-10 of the p53 gene in acute myeloid leukemia patients screened in an epidemiologic study in Brazil were found to correlate with poor prognosis and to occur at frequencies similar to those reported for Northern America and Europe. Mutations in proline 82 of p53 impair its activation by PIN1 and CHK2 in response to DNA damage. Mutations of p53 gene are associated features of aggressive phenotype of transitional cell carcinomas but do not seem to offer additional prognostic information. Mutations of p53 gene were present in 24% (5 of 21) of the evaluable cases, all of them overexpressing p53 in the majority of tumor cells. NDRG1 is necessary but not sufficient for p53-mediated caspase activation and apoptosis. NLS domain of ING4 is essential for the binding of ING4 to p53 and the function of ING4 associated with p53. NO induces the accumulation of transcriptionally active p53 in a variety of cell types and NO signaling to p53 does not require ataxia telangiectasia-mutated (ATM), poly(ADP-ribose) polymerase 1, or the ARF tumor suppressor protein. NPM inhibits hypoxia-induced p53 phosphorylation at Ser-15 and interacts with p53 in hypoxic cells; hypoxia-driven cancer progression may require increased expression of NPM to suppress p53 activation and maintain cell survival. NPM inhibits ionizing irradiation-induced p53 transactivation, and interacts with p53 in hematopoietic cells. New mutations of p53 identified by SSCP in acute myeloid leukemia cell lines. Loss of p53 is not the decisive event causing tumor cells to proliferate in vitro without externally added growth factors. Nitric oxide depletion reduces the presence of p53-DNA complexes after cisplatin treatment. No association between p53 status and overall survival in human glioma. No association was found between the p53 codon 72 polymorphism and rheumatoid arthritis. No somatic mutations were identified in either TP53 or KRAS, indicating that disregulation of these genes is not required for leiomyomas development. Novel gain of function activity of p53 mutants: activation of the dUTPase gene expression leading to resistance to 5-fluorouracil. Nuclear genetic polymorphisms related to oxidative stress or apoptosis may modify the age at onset of Leber's hereditary optic neuropathy (LHON). Nucleophosmin (NPM) interacts directly with p53, regulates the increase in stability and transcriptional activation of p53 after different types of stress, and induces p53-dependent premature senescence on overexpression in diploid fibroblasts. O(6)MeG-triggered apoptosis in proliferating lymphocytes was preceded by a wave of double stranded breaks, which coincided with p53 and Fas receptor upregulation. O-phospho-L-tyrosine protects TP53 wild-type cells against ionizing radiation. One major function of p53 acetylation is to promote p53 stability by preventing MDM2-dependent ubiquitylation, while recruitment of HDAC1 by MDM2 promotes p53 degradation by removing these acetyl groups. Our results indicate that both p73 and p63 may be involved in the development of human buccal squamous-cell carcinoma, perhaps in concert with p53. Out of 110 cases of oral carcinoma, 40 (36%) were p53 positive; p53 over-expression may be involved in only a certain proportion of oral carcinomas. Overexpression of p53 is associated with the pathogenesis of urothelial cell carcinoma. P-53 over-expression can occur in initial stages of HCV-related liver disease. P53 directly inhibits expression of the T cell growth factor (IL-2) in activated T cells. P53 genes from South African esophageal squamous cell carcinoma patients showed: 2 mutations (G>A, codon 331; G>T, donor splice site) in exon 9,4 polymorphisms in intron 3 (16 bp duplication) & exon 4 (C>A, codon 34; G>C, codon 36; G>C, codon 72). P53 is induced by Aluminum in neuron-like cells suggesting that the p53-dependent intrinsic pathway may be responsible for Aluminum-induced apoptosis. P53 is probably involved in the development of conjunctival and eyelid tumors due to its high rate of presence in both benign and malignant neoplasms of these organs. P53 mediates ceramide-induced apoptosis in SKN-SH cells. P53 mutation and LOH on chromosome 17 were found together only in glioblastomas, suggested that these genetic changes may accumulate during astrocytoma progression. P53 mutation predicts the failure of intravesical adriamycin instillation in transitional cell carcinoma of the bladder. P53 overexpression in transitional-cell carcinoma of the kidney pelvis and ureter correlated with tumor-dependent death (p<0.001), tumor proliferation & disease progression, but not histologic grade. P53 protein accumulation may be responsible for gastric carcinogenesis and tumor aggressiveness of gastric cancer in northern China. P53 protein expression and intratumoral microvessel density (IMVD) can be considered as a biological indicator of malignant potential in brain astrocytoma. P53 protein expression in quiescent vascular smooth muscle cells [VSMCs] is paradoxically increased by application of a growth stimulus. Through mediation of p21WAF1/CIP1 and Bax, induced p53 protein negatively regulates the growth of dividing VSMCs. P53 protein overexpression is an early event in esophageal carcinogenesis and useful biomarkers for early detection. P53 protein stimulates calmodulin 2 gene expression in 041 cells. P53 transcriptional activity is inhibited by MDM-2 overexpression, which blocks UV-induced cell cycle arrest and apoptosis. P53-negative AsPC-1 cells are resistant to p53-mediated apoptosis. P72R polymorphism in human papillomavirus associated premalignant laryngeal neoplasm. P73 may replace p53 in triggering not only apoptosis but also cell cycle arrest or DNA repair effectors in breast cancer cells. PARP-1 overexpression counteracts DSB repair independently of its enzymatic activity and of poly(ADP-ribosyl)ation of p53 in particular, but synergizes with p53 in suppressing chromosomal rearrangements. PCAF expression can be induced by wild-type p53. PTEN inhibits MDM2 and protects p53 through both p13k/Akt-dependent and -independent pathways in ALL. PTIP facilitates ATM-mediated activation of p53 and promotes cellular resistance to ionizing radiation. Patients with cancer of the cardiac region had a significantly higher frequency of the Arg/Arg genotype than patients with chronic gastritis, duodenal ulcer, and noncardiac cancer. Patients with tumors who also showed overexpression of p53 had a significantly inferior response to chemotherapy compared with the patients with p53-negative tumors. Peg3/Pw1 is a mediator between p53 and Bax in DNA damage-induced neuronal death. Perturbations of chromosome 17 in general and the p53 locus in particular occur frequently in severe/late stage endometriosis. Phosphorylation of p53 on N-terminal serine residues is not required for increased transcription of most p53-responsive genes. Induction of p53 by p14ARF, with little phosphorylation, leads to substantial repression of genes with roles in proliferation. Phosphorylation of p53 plays a crucial role in detection and interaction with sites of DNA damage and unusual DNA structures. Pifithrin-alpha inhibits p53 signaling after interaction of the tumor suppressor protein with hsp90 and its nuclear translocation. Plays a role in breast cancer in conjunction with BRCA1. Plk3 is a RelA-NF-kappaB-regulated gene that induces apoptosis in both p53-dependent and -independent signaling pathways. Polymorphism at p53 codon 72: A striking reduction in Pro/Pro allele frequency has been found in HPV positive cases, indicating Arg/Arg genotype to be more susceptible to HPV infection and oral carcinogenesis. Probably no association between TP53 polymorphism at codon 72, HPV infection and the etiology of cervical cancer in this population sample. Prognostic significance of p53 mutations in colon cancer at the population level. Proliferative inhibition of breast cancer cells by Velcade is associated with stabilization of p53. Protein tyrosine phosphatase 1-B levels increased with introduction of wt p53 and may be involved in the dephosphorylation of Janus kinase 2. Pseudomonas aeruginosa azurin binds to tumor-suppressor protein p53. Purification, crystallization and preliminary X-ray analysis of the BRCT domains of human 53BP1 bound to the p53 tumour suppressor. Quercetin and ellagic acid combined increase the activation of p53 and p21(cip1/waf1. R273H removes an arginine involved in DNA binding, H168R and R249S induce substantial structural perturbation around the site. RAI3 is a cell growth-promoting gene and a novel P53 transcriptional target. RB18A plays a central role to control p53wt and p53mut protein content and functions in cells through a loop of regulation, which involves MDM2. RNA polymerase III transcription can be derepressed by mutations that compromise p53 function in tumours and Li-Fraumeni syndrome. Substitution R175H, the most common mutation in cancers, converts p53 from a pol III repressor to an activator. Rad51 binds at a promiscuous, highly electrostatic binding site in p53. Radiation induced increased expression of p53. Ionizing radiation induces p53-dependent cell apoptosis in bladder cancer cells with wt- p53 but not in those with mutated p53. Radiation treatment in the presence of p53 C-terminal peptides is more effective for inducing p53 -mediated apoptosis than radiation treatment alone or p53 C-terminal peptide treatment alone in cancer cells. Ras appears to attenuate p53 in SW480 cells by two independent regulatory mechanisms, the one leading to increased Mdm2-dependent p53 degradation and the other leading to a decrease in p53 transcription. Rb and p53 have roles in progression of primary non-small cell lung carcinoma. Recognition of DNA by p53 core domain and location of intermolecular contacts of cooperative binding. Redox state of tumor suppressor p53 regulates its sequence-specific DNA binding in DNA-damaged cells by cysteine 277. Ref-1 promotes association of dimers into tetramers, and de-stacking of higher oligomeric forms into the tetrameric form in vitro, thereby enhancing p53 binding to target DNA. Refolding and structural characterization of the human p53 tumor suppressor protein. Regulation of cyclin E expression plays a role underlying numeral homeostasis of centrosomes in human bladder cancer cells and that deregulation of cyclin E expression, together with inactivation of p53, results in centrosome amplification. Regulation of the nuclear export of hdm2 mRNA provides a mechanism whereby mitogen-stimulated cells avoid p53-dependent cell cycle arrest or apoptosis by maintaining the dynamic equilibrium of the Hdm2-p53 feedback loop. Relation between expression, DNA ploidy and human papillomavirus infection in cervical carcinoma. Relationship between p53 codon 72 polymorphism and susceptibility to sunburn and skin cancer. Repression of hepatocyte nuclear factor 4alpha tumor suppressor p53: involvement of the ligand-binding domain and histone deacetylase activity. Resistance to p53-mediated growth suppression in human ovarian cancer cells retain endogenous wild-type p53. Restoration of wt-p53 activity in Hep3B leads to sensitiveness to chemotherapeutic agents because of the decrease of p-glycoprotein expression. Results are not consistent with a high risk associated with TP53 codon 72 polymorphism in breast and in bladder cancers. Results demonstrated a novel function of Ser(392) phosphorylation in regulating the oncogenic function of mutant p53. Results describe the relationship between Helicobacter pylori (H.pylori) infection and the expressions of the p53, Rb, c-myc, bcl-2 and hTERT mRNA in a series of diseases from chronic gastritis to gastric cancer. Results describe the role of Daxx in modulating the apoptotic threshold and identify it as a possible integrating factor that coordinates the response of p53 family members. Results describe the structural effects of the R249S mutation in the DNA-binding core domain of the tumour suppressor protein p53. Results describe the thermodynamic and kinetic-binding parameters for the interaction between MDM2 and p53 proteins. Results identify a 22-mer peptide derived from the p53 core domain (peptide 14), which inhibits p53-specific DNA binding, and may prevent inappropriately-triggered apoptosis in normal tissues. Results identify a novel mechanism of p53-dependent apoptosis in which p53-mediated up-regulation of MnSOD and GPx, but not CAT, produces an imbalance in antioxidant enzymes and oxidative stress. Results indicate that full-length p53 is a modular protein consisting of defined structured and unstructured regions, which may allow the physiological interaction of p53 with a multitude of partner proteins and the regulation of its turnover. Results indicate that loss of RAR-beta expression and accumulation of p 53 and Ki67 proteins may serve as biomarkers for early identification of esophageal cancer in the high-risk populations. Results indicated that p53 down-regulated the expression of MDM2 oncogene by binding specifically to P3 promoter region. Results link p53 status with POLkappa expression and suggest that loss of p53 function may in part contribute to the observed POLkappa upregulation in human lung cancers. Results obtained in breast carcinoma cell lines indicate that no clear-cut linear relationship exists between the p53 mutational status and the extent of its respective mRNA and protein expression. Results showed significant differences in the expression patterns among p53-null. wild-type p53, and p53 mutants A138T, C141Y, R158L, G245C, and R248Q samples. We also report here the first found p53 mutant-triggered alternative splicing. Results showed that mutations in the p53 gene were frequently detected in in recurrent hepatocellular carcinoma. Results suggest that apoptosis-associated speck-like protein (ASC) can function as an adaptor molecule for Bax and regulate a p53-Bax mitochondrial pathway of apoptosis. Results suggest that intrinsic DNA binding affinity and p53 protein levels are important contributors to p53-induced differential transactivation. Results suggest that p53 degradation and inhibition of p14(ARF) signaling are independent functions of HPV16 E6, and that long-term proliferation of mammary epithelial cells requires inactivation of the p14(ARF)-p53 pathway. Results suggest that progression of esophageal squamous cell carcinoma is controlled by a p53-dependent pathway. Results suggested that the loss of p53 expression in conjunction with the overexpression of p21(WAF1/CIP1) was a stronger predictor of survival benefit than either molecule alone in Japanese serous-type advanced ovarian cancer. Resveratrol caused a dose-dependent increase in intracellular p53 and p21(WAF1/CIP1) levels. Resveratrol enhances the expression of non-steroidal anti-inflammatory drug-activated gene (NAG-1) by increasing the expression of p53. Review focuses on potency of p53 as an inducer of apoptosis and reasons for extraordinarily high frequency of p53 inactivation in tumors, and mechanisms of tumor cell sensitization to p53-induced apoptosis. Review outlines uses of adenoviruses in brain tumor therapy by examining clinical trials of adenovirus-mediated p53 gene therapy and by reviewing the application of two conditionally replicative adenoviruses (CRAds) ONYX-015 and Delta 24 in brain tumors. Review. the role of p53 post-translational modifications in carcinogenesis and cancer prevention. Role of p53 domains in binding to supercoiled DNA. SAK repression by p53 is likely mediated through the recruitment of HDAC repressors, and SAK repression contributes to p53-induced apoptosis. SCN3B mediates a p53-dependent apoptotic pathway and may be a candidate for gene therapy combined with anticancer drugs. SN2 DNA-alkylating agent-induced phosphorylation of p53 increases its DNA-binding properties to cause an increased expression of p21 that may play a role in cell cycle arrest and/or apoptosis of human colon cancer cells HCT-116. STAG1, a novel transcriptional target for p53, mediates p53-dependent apoptosis, and might be a good candidate for next-generation gene therapy in cancer. SV40 large T antigen associates with a cellular phosphoprotein, p53, in virus-transformed cells.Monoclonal antibodies, PAb1101, PAb1102 and PAb1103 define at least two non-overlapping determinants on human p53. Selection pressures of TP53 mutation and microenvironmental location influence epidermal growth factor receptor gene amplification in human glioblastomas. Sequential extension of proliferative lifespan in human fibroblasts is induced by over-expression of CDK4 or 6 and loss of p53 function. Serine 392 exerts important effects upon p53 stability via the inhibition of its nuclear export mechanism. Simulated sunlight and benzo[a]pyrene diol epoxide induced mutagenesis in the human p53 gene. Specific silencing of p53 abrogated the antiviral effect of SD.IFN-beta, suggesting that the tumor suppressor is critically involved in antiviral defense mediated by intracellular IFN. Squamous cell carcinoma of the head and neck shows a high incidence of p53 tumor suppressor gene alterations; the latter therefore appears to play an important role in the pathogenesis and progression of such neoplasms. Status of gene affect and nature of chromosome damage seen in human skin fibroblasts after gamma irradiation beyond the G1-phase checkpoint but prior to the G2-phase checkpoint. Stress-induced activation of p53 in leukemia cells and normal lymphocytes requires mitochondrial activity and reactive oxygen species. Structural analysis shows that the high stability of the Ser116Met modeled mutant is due to the preservation of the p53 core domain loop L1 conformation and the reduction of mobility in that region. Study indicate that the coexistence of p53 protein accumulation and HER2 overexpression is a strong prognostic molecular marker in breast cancer. Study reports the first unequivocal case of a ganglioglioma harboring aberrant TP53 product that was expressed predominantly in the neuronal component. Syncytia from cells expressing the HIV-1 Env gene fused with cells expressing CD4/CXCR4 undergo apoptosis after nuclear translocation of mTOR, mTOR-mediated p53 phosphorylation, p53-dependent Bax upregulation & mitochondrial death pathway activation. T-oligos transcriptionally down-regulate COX-2 expression in human skin via activation and up-regulation of p53, at least in part by inhibiting NFkappaB transcriptional activation. TFII-I is degraded in a p53-dependent manner and this degradation may contribute to p53-induced cell cycle arrest. TIAF1 and p53 functionally interact in regulating apoptosis, and TIAF1 is likely to participate in the nuclear translocation of activated p53. TP53 arginine/arginine genotype could represent a potential risk factor for the development of squamous cell carcinoma in renal transplant recipients. TP53 deletion significantly associated with malignant transformation of breast papilloma, pointing to p53 role as a progression factor. TP53 does not have a role in the histologic response to chemotherapy in patients with osteosarcoma, but its mutation may be associated with disease progression. TP53 expression may be a useful biomarker for assessing the risk of developing esophageal cancer. TP53 function closely influences the decision between apoptosis and growth arrest following Fatty acid synthase blockade. TP53 has a role in aortal endothelial cell aging. TP53 inactivation is a major mechanism of HPV-related carcinogenesis in the oral cavity and oropharynx. TP53 is regulated by superoxide dismutase 1 in human cells. TP53 is ubiquitinated by topors. TP53 mutation frequently occurs in higher stages of bladder tumours. TP53 mutation has only a limited role in the transformation of lymphoma to diffuse large B-cell lymphoma, exerting a heterogeneous influence upon phenotypic change. In contrast, dysregulation of MDM2 is frequent. TP53 mutation is common in early stage ovarian carcinomas of serous histology, with a mutation frequency comparable to that reported for advanced-stage ovarian tumors. TP53 mutations could be a useful prognostic indicator in precancerous oral lesions. TP53 mutations develop in non-neoplastic epithelial lesions of the vulva, lichen sclerosus and squamous hyperplasia and are intrinsic to the clonal evolution that leads to squamous cell carcinoma of the vulva. TP53 mutations in breast cancer tumors of patients from Rio de Janeiro, Brazil: association with risk factors and tumor characteristics. TP53 mutations were associated with high-stage, high-grade urothelial carcinomas of the bladder. TP53 pathway is invslved in the carcinogenesis ofHepatic undifferentiated (embryonal) sarcoma. TP53 polymorphisms were characterized in a cohort of 779 patients, of whom 342 cases had developed restenosis at six months post PTCA. TP53 rearrangements in families with the Li-Fraumeni syndrome reveals a complete deletion of the TP53 gene. TP53-mediated transcription is induced by prohibitin in human tumor cells through enhanced recruitment to promoters. TP53-mutated tumors need fewer additional genetic alterations to develop metastases in primary head and neck tumors compared with TP53 wild-type primary tumors. TP53INP1s and HIPK2 could be partners in regulating p53 activity. TRR-Trx and APE/Ref-1 cooperate in the control of basal p53 activity, but not in its induction by DNA-damage. TSG101 expression in gynecological tumors: relationship to cyclin D1, cyclin E, p53 and p16 proteins. Taken together, these results suggest a novel function of COX-2 that inhibits DNA damage-induced apoptosis through direct regulation of p53 function. Taking p53 negativity in immunohistochemistry as evidence of a functional gene/protein, this extends the link between proliferation and apoptosis, hitherto observed only in cultured cells with functional p53, to a subset of solid tumours. Targeted inactivation of p53 in human cells does not result in aneuploidy. Telomerase activity in microdissected human breast cancer tissues: association with p53, p21 and outcome. The 3' UTR of p53 was found to be a target of the RNA-binding protein HuR in a UVC-dependent manner in vitro and in vivo. The Aberrant expression of p53 Genes were determined in bone marrow samples of children with de novo B-lineage (n=170) and T-lineage (n=25) acute lymphoblastic leukemia (ALL). The HIF-1alpha ODD domain binds weakly to the isolated p53 core domain but tightly to full-length p53 to give a complex of one HIF-1alpha ODD domain with a p53 dimer. The N-terminal domain of p53 is natively unfolded. The ability of p53 to bind and inactivate JNK, together with the activation of the p53 target genes related to cell cycle arrest and DNA damage repair, is responsible for its protection of cells against UV-induced apoptosis. The ability to form unique amphipathic structures in both an aqueous cytosolic-like and a mixed organic membrane-mimetic solution environment may allow a p53 peptide from the mdm-2 binding domain to selectively and rapidly disrupt cancer cell membranes. The activation of the p53 pathway appears to be an effective approach in inhibiting tumor development. The antiproliferative properties conjugated linoleic acids are a function their ability to elicit a p53 response that leads to the accumulation of pRb and cell growth arrest. The candidate tumor suppressor ING1b can stabilize p53 by disrupting the regulation of p53 by MDM2. The capability of p53 to activate transcription was used to develope a new assay that permits rapid determination of the status of p53 in cancer cell lines of different origin. The combination of mutation with the codon 72 proline variant predicts poorer patient survival in non-small cell lung cancer. The complement inhibitor CD59 and the lymphocyte function-associated antigen-3 (LFA-3, CD58) genes possess functional binding sites for the p53 tumor suppressor protein. The coupled folding and binding of the p53 transactivation domain to the 70 kDa subunit of human replication protein A was investigated. The coupled induction of iNOS and p53 upregulation in intrinsic renal cells of IgA nephropathy may be linked with both pro- and anti-apoptotic activities. The data was obtained that establishes the contribution of the transcription-independent mitochondrial p53 pathway to apoptosis of primary cells in response to deregulated oncogenes. The detected pattern of the p53/ bcl-2 ratio in hypertrophic actinic keratosis suggests important role for another gene: the proapoptotic gene bax. The detection of mutant p53 protein in hepatocellular cancer is corellated with clinicopathologic parameters and incidence of the liver neoplasms in Turkey. The expression of bcl-2 and p53 represent biological characteristics of colorectal carcinomas. The expression of p21 protein depends on p53 protein largely in normal gastric mucosa and dysplasia, but not in gastric carcinoma. The finding of different p53 gene mutations among multiple esophageal carcinoma lesions suggest further evidence of multicentric or field carcinogenesis of the human esophagus. The first direct demonstration of p53 mutations in pleuropulmonary blastomas (PPB)suggests p53 inactivation can occur as a nonrandom genetic change involving the pathogenesis and outcome of PPB. The frequency of p53-positive patients is relatively low in T-ALL (29%) and B-CLL (16%). B-ALL, AML and CML patients revealed higher frequency of p53 protein. The frequent presence of TP53 deletion detected in 48% of patients is surprising. It is generally thought that the aberration is found in 10-15% of clinical cases. The homeodomain of Msx1 functions as a protein-protein interacting motif rather than a DNA-binding domain and is essential for stabilization, nuclear accumulation, and apoptotic function of wild-type p53. The human gene in transgenic mice behaves like its murine ortholog in mouse hepatocarcinogenesis. The immunodetection of both p53 and bcl-2 proteins in squamous cell carcinoma of the uterine cervix can be used as an independent diagnostic marker for cervical cancer associated with HPV infection. The lack of Bcl2 accompanied by p53 overexpression affects the distribution of cells among the cell cycle phases and modifies the sensitivity to cytotoxic drugs and the type of cell death. The levels of p53 protein elevated in keloid, hypertrophic scar and white and hard hypertrophic scar. The low-molecular-weight compound PRIMA-1 restored sequence-specific DNA binding and the active conformation to mutant p53 proteins in vitro and in living cells. The major lipid peroxidation product, trans-4-hydroxy-2-nonenal, preferentially forms DNA adducts at codon 249 of human p53 gene, a mutational hotspot in hepatocellular carcinoma. 4-HNE may cause human cancers with mutations at codon 249 of p53 gene. The mechanism of action of apigenin seems to involve p53, as it increased the levels of p53 and the p53-induced gene products p21WAF1/CIP1 and Bax. The p21 upregulation followed the p53 phosphorylation process in irradiated MOLT-4 ce. The p53 Pro allele is associated with an increased frequency of p53 mutations in non-small cell lung cancer. The p53 codon 72 gene polymorphism is not associated with the susceptibility of leiomyomas. The p53 codon 72 polymorphism is unlikely to be related to HPV status and the onset of cervical cancer. The p53 genotype distribution was markedly different between the ovarian mucinous cystadenocarcinomas and serous papillary cystadenocarcinomas with respect to homozygosity of both Arg and Pro. The p53 overexpression was an important factor in the process of carcinogenesis of elder women with cervical cancer and a predictive indicator for lymph node status. The p53 tumor suppressor pathway is disrupted in most oral squamous cell carcinomas at the cellular levels, due to either an abnormality in p53 itself or loss of expression of p53 regulatory factors. The p53Arg allele was not associated with the development of cutaneous SCC. The point mutation of p53 gene exon7 in hepatocellular carcinoma from Anhui Province, a non HCC prevalent area in China. The poor prognosis associated with p53-null mutation is independent of the mutation mechanism in ovarian cancer survival. The positive expression rates of p21 and p53 proteins were 75.0% and 57.3% respectively in pancreatic carcinoma, which were significantly different from those in the normal tissue (P<0.05). p21 and p53 proteins were positively correlated (P<0.05). The presence of E-cadherin mutations can significantly alter the accumulation of the apoptosis-regulating p53 protein, whereas no correlation with the p53 mutation status or with Ki-67 staining was observed. The presence of wild-type p53 increased survival of prostate carcinoma cells after fractionated exposure to radiation. The prolyl isomerase Pin1 is a regulator of p53 in genotoxic response. The relationships and interactions between p53, Rb and bcl-2 immunostaining, clinical parameters and response to cisplatin-based chemotherapy were evaluated in the present study. The restoration of wild-type p53 expression and function in human autologous lung carcinoma IGR-Heu cells results in a significant potentiation of target cell susceptibility to cytotoxic T cell-mediated lysis. The results showed that retroviral vector-mediated RNAi can substantially downregulate the expression of human p53 in 293-T cells. The results suggest that I3C represses cell proliferation through up-regulation of NAG-1 and that ATF3 may play a pivotal role in DIM-induced NAG-1 expression in human colorectal cancer cells. The sequential accumulation of mutations in p53 drives the transition from normal epithelium through increasing adenomatous dysplasia to colorectal cancer. The suppression of STK15 oncogenic activity by p53 might be explained by the finding that p53 inhibited STK15 kinase activity via direct interaction with the latter's Aurora box. This revealed a novel mechanism for the tumor suppressor function of p53. The temperature sensitive mutant p53-143ala extends in vitro life span, promotes errors in DNA replication and impairs DNA repair in normal human oral keratinocytes. There is some evidence that p53 is involved in the regulation of XPE DDB2 or XPC. There was a differential upregulation of p53-responsive genes by genotoxic stress in hematopoietic cells containing wild-type p53 (MOLT-4) or a mutant p53 with a codon 161 mutation (U266). There was no correlation between human papillomavirus status and p53 overexpression in human oropharyngeal squamous cell carcinoma. These data indicate a novel p53-dependent mechanism in which cell stress mobilizes nucleolin for transient replication inhibition and DNA repair. These data suggest that nucleophosmin is an early responder to DNA damage that prevents premature activation of p53. These findings suggest that impairment of transcriptionally active p53 in response to replication blockade is not a general phenomenon. These results are consistent with a model in which p53 and Mcl1 have opposing effects on mitochondrial apoptosis by interacting with, and modulating the activity of, the death effector Bak. These results demonstrate direct activation of the human DDB2 gene by p53. The corresponding region in the mouse DDB2 gene shared significant sequence identity with the human gene but was deficient for p53 binding and transcriptional activation. These results demonstrate that butyrate inhibited the growth of breast cancer cells in a P53-independent manner. These results demonstrate that overexpression of Activating transcription factor 3 (ATF3) suppresses tumor necrosis factor-alpha-induced cell death of HUVECs, at least in part, through down-regulating the transcription of p53 gene. These results have important implications regarding the mechanism of tumorigenesis involving missense p53 mutants or the N-terminally truncated isoforms. These results indicate that p53 and BLM functionally interact during resolution of stalled DNA replication forks and provide insight into the mechanism of genomic fidelity maintenance by these nuclear proteins. These results reveal that ribosomal protein L23 is another regulator of the p53-MDM2 feedback regulation involved in cell growth. These results suggest that Chk2 regulates the transcription-independent mechanism of p53-mediated apoptosis by inducing stabilization of p53 in response to IR. These results suggest that p53 is vulnerable to free radical-mediated oxidation at cysteine residues. These results suggest that p53 might modulate the repair of DNA adducts generated from the human bladder carcinogen ABP in its target human uroepithelial cells. These results suggest that the expression of eIF4E is reciprocally regulated by p53. This additivism, where doxorubicin acts via p53 expression and vinorelbine through p38 MAP KINASE activation, may contribute to the high clinical response rate when the two drugs are used together in the treatment of breast cancer. This gene is mutated in breast cancer. This protein and p73 interact with CTF2 and regulate HMG1 gene expression. This protein interacts with TFAM and helps regulate DNA damage. This protein is required for the Nuclear localization of Y-box factor YB1. This study focused on the expression levels of Bcl-2 family regulators (anti-apoptotic Bcl-2 and Bcl-XL, pro-apoptotic Bcl-Xs and Bax), p53, and PCNA as a marker of proliferation, together with the evaluation of the level of apoptosis in human embryos. This study observes statistically significant differences on SNP rs2078486 and on haplotype CAC. These results demonstrated that TP53 might play a role in susceptibility to schizophrenia. Three novel TP53 mutations found in Russian breast cancer patients. Three point mutations of p53 gene were not predictive for tumor development in liver and renal transplantation patients. Through a combination of induced p53 aggregation and diminished site-specific DNA binding activity, Zn2+ loss may represent a significant inactivation pathway for p53 in the cell. Thus, the accumulation of mutant p53 in tumor cells may contribute to tumorigenesis by inhibiting stress-inducible kinase pathways. Tip60 plays a double role in the p53 pathway: under normal growth conditions, Tip60 contributes to maintain a basal pool of p53 by interfering with its degradation; following DNA damage, Tip60 functions as p53 co-activator. Tissue samples from 42 ulcerative colitis patients were evaluated for p53 alterations by immunohistochemistry, loss of heterozygosity analysis, polymerase chain reaction-single-strand conformation polymorphism and direct sequencing. To determine whether genotoxic stress regulates DNA binding by p53 in vivo, we have performed quantitative chromatin immunoprecipitation (ChIP) assays on tumor and normal cell lines containing wild-type p53. Transactivation-deficient Delta TA-p73 inhibits p53 by direct competition for DNA binding: implications for tumorigenesis. Transactivation-dependent apoptosis does not always play a major role in p53-dependent apoptosis, indirectly supporting the importance role of the transactivation-independent mechanism. Transcriptional activity depends on p53 and BRCA1: inability of the mutant suppressor to repress IGF-IR expression result in increased IGF-IR levels and IGF binding. Transcriptionally active p53 is required for nuclear localization of Y-box-binding protein (YB1). TrkA induces apoptosis of neuroblastoma cells and does so via a p53-dependent mechanism. Tumor cell killing by autologous cytotoxic T lymphocytes can be enhanced by targeting degranulation-independent mechanisms via restoration of wild-type p53, a key determinant of apoptotic machinery regulation. Tumor cells with wild-type p53 activity exhibited up-regulation of surface CD95 after ionizing irradiation. Tumor protein p53, a nuclear protein, plays an essential role in the regulation of cell cycle, specifically in the transition from G0 to G1. It is found in very low levels in normal cells, however, in a variety of transformed cell lines, it is expressed in high amounts, and believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing DNA-binding, oligomerization and transcription activation domains. It is postulated to bind as a tetramer to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and hence cause the loss of tumor suppressor activity. Alterations of the TP53 gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome. Tumor-derived p53 mutants increase the cell growth rate. They cannot bind the wild-type p53 consensus sequence. The mutants have 'gain of function' properties. D281G transactivates asparagine synthetase & human telomerase reverse transcriptase promoters. Tumorigenesis pathway independent of p53 dysfunction appears to exist in association with ulcerative colitis. Twist-overexpressing MCF-7 cells displayed a deregulated p53 response to gamma-radiation and decreased regulation of downstream target genes. Two cases of lymphomatoid palulosis with mutated p53 gene in biopsy showed no progression of disease in 5 yr follow up. May not play any significant role in the pathogenesis, progression or transformation of cutaneous CD30(+) lymphoproliferative diseases. Two peptide epitopes on Mdm2 oncoprotein affect this protein's degradation. UV-induced DNA damage in epidermal KCs triggers p53 activation and apoptosis. Lack of activation in aging KCs and psoriatic Regulation of apoptosis by p53 in UV-irradiated human epidermis, psoriatic plaques and senescent keratinocytes. UV-induced activation of p53R2 transcription and binding of p53R2 to hRRM1 to form RR holoenzyme are impaired in the p53-mutant cell line PC3. UVB-mediated activation of p38 mitogen-activated protein kinase enhances resistance of normal human keratinocytes to apoptosis by stabilizing cytoplasmic p53. UbcH5B/C are E2s for Mdm2, which contribute to the maintenance of low levels of p53 and Mdm2 in unstressed cells; inhibition of p53 ubiquitination and degradation by targeting UbcH5B/C is not sufficient to up-regulate p53 transcriptional activity. Ubiquitination and degradation of p53 are largely controlled by Mdm2, an oncogenic E3 ligase. Under severe hypoxic conditions p53 protein accumulates only in S phase; this correlates with replication arrest. Inhibition of ATR kinase activity substantially reduces hypoxia-induced phosphorylation of p53 protein on ser 15 as well as p53 accumulation. Unique repressor domain resides in p53 at residues 90-116 whose activity can be modulated in the presence of 'differentiation therapy' and 'transcription therapy' agents. Upregulation of p14ARF paralleled with MDM2 inhibition contributes to p53 accumulation in the nucleus in radiation-treated breast cancer cells. Upregulation of p53 protein is associated with breast disease. VEGF and p53 are highly expressed in esophageal carcinomas. VEGF expression plays a role in promoting angiogenesis in invasive ductal carcinoma of the breast, and p53 is likely to be involved in regulating VEGF expression. VHL-mediated p53 upregulation may contribute to pVHL's tumor suppressive functions in renal cell carcinoma. VRK1 is the first step in a new pathway regulating p53 activity during cell proliferation. Vascular endothelial growth factor (VEGF) expression correlates with p53 and ki-67 expressions in tongue squamous cell carcinoma. WOX1/p53 has a potential role as a signaling complex in mitochondrial apoptosis. WR1065 specifically modulates a subset of p53 target genes in a colon carcinoma cell line, consistent with the observation that this agent elicits essentially p53-dependent, cell cycle arrest responses. WRN and TP53 perform different functions in a shared DNA damage response pathway. We conclude that (1) clinically achievable doses of ionizing radiation can trigger CDKN1A-dependent accelerated senescence in some human tumor cell lines that express wild-type TP53. We conclude that overexpression of PKCdelta in human colon cancer cells induces multiple antineoplastic effects that depend on the activities of p21(Waf1/Cip1) and p53. We found mutations in p53, K-ras, and BRAF genes in 35%, 30%, and 4% of tumors, respectively, and observed a minimal or no co-presence of these gene alterations. We investigated three common sequence variants in TP53 and p21 for possible associations with the risk of breast cancer and with various phenotypic features of this disease. We probe the significance of mitochondrial p53 and show that tumor-derived transactivation-deficient mutants of p53 concomitantly lose the ability to interact with BclXL and promote cytochrome c release. We propose that induction of NQO2 may relate to the observed increased expression of p53 that, in turn, contributes to the observed suppression of cell growth in both melanoma cell lines. We show a novel alternative pathway of apoptosis in human primary cells that is mediated by transcriptionally dependent decreases in p53 and c-Myc and decreases in p21. We thus identified ik3-2 as a proapoptotic factor involved in both p53-mediated and p53-independent apoptotic pathways. Wild-type and mutated presenilins 2 trigger p53-dependent apoptosis and down-regulate presenilin 1 expression in HEK293 human cells and in murine neurons. Wild-type p53 protein conformation is stabilized upon CP-31398 exposure. Wild-type p53 regulates human ribonucleotide reductase by protein-protein interaction with p53R2 as well as hRRM2 subunits. With respect to overexpressed p53 a significant difference was reached for complete remission rate (P = 0.01) and 5-year survival rate. YY1 regulates the transcriptional activity, acetylation, ubiquitination, and stability of p53 by inhibiting its interaction with the coactivator p300 and by enhancing its interaction with the negative regulator Mdm2. Zinc deficiency caused an increase in p53 protein expression. A correlation between focal p53 immunostaining in primary primary prostate cancers and cancer recurrence after radical prostatectomy. A new T-->C point mutation was identified in intron 6 at position 13989 in a grade III medullary ductal breast carcinoma. A novel p53-dependent mechanism in the PPARgamma ligand-mediated inhibition of cholangiocarcinoma growth and suggest a potential therapeutic role of PPARgamma ligands in the treatment of human cholangiocarcinoma. A productive human herpesvirus 6B infection suppresses T-cell proliferation concomitant with the phosphorylation and accumulation of p53. A transcriptional switch from P(0)-/P(2)- to P(1)-initiated p53 mRNA could be an important mechanism by which cells regulate p53 expression. Aberrent expresion correlates with VEGF and IL-8 mRNA expression and neoangiogenesis in non-small-cell lung cancer. Abnormal expressions of COX-2, p53, PCNA, and nm23 associate with malignant potential, lymph node metastasis and clinical stage, and they might therefore play a role in development of gastric cancer. Abrogation of p53 functional activity can be a common feature of MLL fusion-mediated leukemogenesis. Acetylation of p53 activates transcription through recruitment of coactivators/histone acetyltransferases. Acetylation of the C-terminal domain is sufficient to abrogate its ubiquitination by Mdm2. Activates ICAM-1 (CD54) expression in an NF-kappaB-independent manner. Activation of the DNA DSB checkpoint provides the selective pressure for the high frequency of p53 inactivation in human cancer [review]. Activation of the p53-p21WAF1 pathway and overexpression of cyclin D1 are induced during tumor cell differentiation by beta-catenin. Adenovirus 2 E1B-55K protein blocks p53 as a transcriptional repressor protein of the survivin and the MAP4 promoters. Alterations in both p53 and p16ink4a can contribute to recessive dystrophic epidermolysis bullosa-associated squamous cell carcinoma. An aberrant p53 status was related to IL-8 expression in patients with non-small cell lung carcinoma. An apoptosis-deficient Pro allele of the p53 gene may be related to psoriasis resistance to UV-based therapy. An over-representation of the Pro allele of the p53 gene in women with idiopathic recurrent miscarriage gives support to the theory that p53 has a potential role during pregnancy. Analyses of statistical interactions between polymorphisms (p73 G4A, p53 Arg72Pro and p21 Ser31Arg polymorphisms) revealed the marginally significant risk of non-Hodgkin's lymphoma for interaction between p53 Arg72Pro and p73 G4A polymorphisms. Analysis of the role of HTLV I Tax in p53 inhibition in leukemia [review]. Association between genetic polymorphisms of GSTT1, p53 codon 72 and bladder cancer in southern Taiwan. Azurin, tumor suppressor protein p53, and regression of cancer. Basal expression of p53 plays a functional role in a glucocorticoid receptor-mediated response regulating the expression of p21(Waf1/Cip1) via a mechanism that is suppressed by PP5 and associated with the phosphorylation of p53 at Ser-15. Basal p53 expression in WI38 human embryonic lung fibroblasts restricts growth rate and mediates density-dependent inhibition of growth and the associated G1 phase arrest of the cell cycle by affecting the density-dependent regulation of p16/INK4a. Bcl-2 may inhibit cell death at multiple points downstream of p53 activation. Bcl-2/Jh lymphomas show molecular heterogeneity and that bcl-6 and p53 mutations may be acquired during the evolution of such lymphomas. Besides P53 alterations, mouse double minute 2 gene deregulation seems to be an important event in hepatocarcinogenesis. Beta-catenin, p53 and PCNA may play important roles in the carcinogenesis of colorectal adenoma. Binding and activation of PIG3 promotoer via a pentanucleotide microsatellite sequence. Binding sites of 53BP1. Biogenesis in vitro to determine how wild type and mutant forms form hetero-oligomers. Blockade of pol II-mediated transcription induces p53 accumulation in mitochondria and is the critical factor for eliciting p53-dependent but transcription-independent apoptosis. Both HPV infection and p53 gene abnormalities may contribute to Bilharzial bladder carcinogenesis in an independent way. By binding to E6, Pitx2a interferes with E6/E6AP-mediated p53 degradation, leading to the accumulation of functional p53 protein in HeLa cells. Cell lines that contain human tumor-derived temperature-sensitive p53 mutants show that Hsp90 is required for both stabilization and reactivation of mutated p53 at the permissive temperature. Central and carboxy-terminal regions are essential for interaction and complex formation with PARP-1. Cloned and characterized a p53 consensus element located within the first intron of the TRAIL-R3 gene. Codon 47 polymorphism of p53 is functionally significant and may play a role in cancer risk, progression, and the efficacy of therapy. Colocalization of a nonshuttling p53 with MDM2 either in the nucleus or in the cytoplasm is sufficient for MDM2-induced p53 polyubiquitination but not degradation. Combination of protein p53 induction and ionizing radiation activate the proliferating cell nuclear antigen gene. Combined expression of p53 and metallothionein did not improve the predictive value for recurrence compared to MT alone. Complete loss of p53 is a prerequisite for collaborating with activated Ha-ras to promote bladder tumorigenesis. Cyclin K is targeted for transcription by p53. Cytoplasmic localization is stimulated my GTSE-1 expression. Cytoplasmic sequestration of p53 by the E1B 55-kDa protein plays an important role in restricting p53 activities in human osteosarcoma cells. Data suggest that p53pSer15 plays a dual role in the functional interactions with early complexes of Rad51-dependent recombination and with BLM-associated surveillance and signalling complexes within distinct nuclear subcompartments. Deacetylase HDAC1 acts as an antagonist of the tumor suppressor p53 in the regulation of the cyclin-dependent kinase inhibitor p21. Deacetylated p53 can transactivate the p21Waf1 gene. Decreased cell-surface expression of Fas and resistance to Fas-mediated apoptosis may occur independently of loss of wt p53 expression in esophageal adenocarcinoma. Demonstrated that a tripartite nexus between Bcl-xL, cytoplasmic p53, and PUMA coordinates the nuclear and cytoplasmic p53 proapoptotic functions. Demonstrated that epigallocatechin-3-gallate activates growth arrest and apoptosis primarily via tumor suppressor p53-dependent pathway that involves the function of both p21 protein and Bax protein. Describes that lactoferrin specifically transactivates the p53 tumor suppressor gene through the activation of nuclear factor-kappaB and consequently regulates p53-responsive oncogenes. Description of a novel MDM2 binding interface in p53 that plays a regulatory role in MDM2-dependent ubiquitination of p53. Description of the role of ionic interactions in the stability of the p53 tetramer and of heterotetramers of the protein scaffold. Different genotype combinations of p53 and GSTM1 increase the risk of developing specific histological subtypes of NSCLC. Differentiation status of the tumor was found for the p53 aberration but not for CD95 expression. Disrupted p53/BAX pathway is associated with a poor clinical outcome in UICC III tumors. Downregulation of Cdc25C is mediated by p53 via two independent mechanisms, one involving direct binding to the cdc25C promoter. EIF5A may be a regulator of p53, and syntenin might regulate p53 by balancing the regulation of eIF5A signaling to p53 for apoptosis. Effect of HCV core, NS3, NS5A and NS5B on cell proliferation is independent of p53 expression, and only HCV core protein induces the expression of both c-myc and p53. Effect of phosphorylation on structure and fold of transactivation domain. Elevated levels of Myc counteract p53 activity in human tumor cells. Enhanced microtubule-dependent trafficking and p53 nuclear accumulation by suppression of microtubule dynamics. Epidemiological study suggests a role for p53PIN3 in tumorigenesis. Estimation of the sensitive positions to mutations in human p53 protein. Estradiol induces variations of p53 protein levels in epithelial cancer-derived cell lines from the reproductive tract in vitro; this may be related with status p53 and/or presence of E6/E7 from human papillomavirus [review]. Evidence that in lung carcinomas, non-CpG methylation is frequently observed in certain GC rich regions of the p53 gene; evidence presented from the p53 mutation databases which corroborates the reported experimental results. Examination of expression of p53, p21, and phosphorylated p42/44 mitogen-activated protein kinase in human pulmonary arterial smooth muscle cells. Examined the binding of DNA in solution to a series of unmodified p53 constructs that lack various domains, and identified the residues of the C terminus that interact with the non-specific DNA. Exposure-specific heterogeneity in inactivation of the TP53 pathway in bladder cancers. Expressed in biopsies from children with Langerhans cell histiocytosis. Expression has an independent effect on prediction of survival, progression, and development of metastasis in transitional cell bladder carcinoma. Expression in pelvic lymph nodes and primary tumors in early stage cervical carcinomas. Expression of apoptosis-regulating proteins p53, Bcl-2, and Bax in primary resected esophageal squamous cell carcinoma. Expression of iNOS, P53 and Bax in the gallbladder wall. Expression of p21/CDKN1A is necessary and sufficient for the negative regulation of gene expression by p53. Expression of p53 is essential for cytotoxic effect of cisplatin in human malignant glioblastoma cells, A172 and T98G, and introduction of apoptotic signal molecules, such as p53, will be beneficial to achieve chemosensitivity in malignant glioma. Expression of telomerase genes (hTR, hTRT) and apoptosis related genes (p53, bcl-2) in mammary atypical ductal hyperplasia. Findings suggest a novel mechanism of MLH1 in the induction p53 and apoptosis by inhibiting RNA polymerase II-dependent transcription on damaged DNA templates. Findings suggest that the Pro/Pro genotype of p53 codon 72 played a role in prostate cancer susceptibility in a Japanese population; the Pro allele did not appear to worsen such clinical parameters as clinical stage or pathological grade. Findings suggest that the tumor protein p53 codon 72 polymorphism is unlikely to be associated with endometriosis in Japanese women. First demonstration in human cancer cells that the p53 pathway can be suppressed by factors in the tumour-cell microenvironment. Following stress-induced phosphorylation, p53 needs to form a complex with Pin1 and to undergo a conformational change to fulfil its biological roles. Forced p53 gene expression is cytotoxic to human bladder cancer cells with either p53 mutant or wild-type background. Functions of p53 in regulating gene expression that play both synergistic and pleiotropic roles in p53-associated apoptosis. Generation of the polyubiquitinated forms of p53 that are targeted for proteasome degradation requires the intrinsic ubiquitin ligase activities of MDM2 and p300. Germline mutations in the TP53 gene in five index cases of German and Swiss origin with cancers typical of Li-Fraumeni syndrome. HHR23 binds to polyubiquitylated p53 via its carboxyl-terminal ubiquitin-associated (Uba) domain shielding p53 from deubiquitylation. HMdmx is overexpressed in a significant percentage of various human tumors and amplified in 5% of primary breast tumors, all of which retained wild-type p53. iRNA-mediated reduction of hMdmx inhibited cell growth potential in a p53-dependent manner. HNRAGE arrests cell growth through a p53 dependent pathway. hNRAGE also increases the p53 protein level as well as its phosphorylation (Ser392). Half-life (t(1/2)) of the unfolding of highly destabilized mutants. Heat shock stabilization by phosphorylation and heat shock protein 90 binding. Hepatitis B virus X protein on the regulation of cell-cycle control depending on the status of cellular p53. Hepatitis C virus core protein induces p53-dependent gene expression of TAP1 protein and MHC class I upregulation in liver cells and thus impairs NK cell cytotoxicity. Herpesvirus saimiri (HVS) ORF73 binds both p53 and pRb in vitro and in vivo, colocalizes with p53 in T cells infected with HVS, and in cells overexpressing both ORF73 and p53, and adversely influences pRB/E2F and p53 transcriptional regulation. High level of p53 protein in cPNETs measured by immunostaining intensity associated with poor patient survival. Higher expression in atrophic oral lichen planus and patients with areca quid chewing. Higher expression in childhood leukemias with poor prognosis compared to long-term survivors. Higher frequency of spicy food intake and use of unboiled well water may be risk factors of esophageal cancer via p53 mutations in China. Hsp90beta is repressed by p53 in UV irradiation-induced apoptosis. Hyperoxia activates the ATR-Chk1 pathway and phosphorylates p53 at multiple sites in an ATM-independent manner, which is different from other forms of oxidative stress such as H2O2 or UV light. Identification of defect in response pathway induced by de novo purine synthesis inhibition. Identification of one known and five new modulators of p53-dependent proliferation arrest, using an RNA interference library. Identified a global suppressor motif involving codons 235, 239, and 240. Identified executioner caspase-6 as a transcriptional target of p53. The mechanism involves DNA binding by p53 to the third intron of the caspase-6 gene and transactivation. Immunohistochemistry and PCR-SSCP analysis of p53 are useful for pathological discrimination between UC-associated neoplasia and inflammatory regenerative epithelium; may contribute to accurate endoscopic detection of UC-associated neoplasia. In cell lines containing inducible versions of alleles encoding the Pro72 and Arg72 variants, and in cells with endogenous p53, the Arg72 variant induces apoptosis markedly better than does the Pro72 variant. In oral cancer cells the Ca(2+)- and cell cycle-dependent p53-S100A2 interaction might modulate proliferation. In progeria, the premature ageing phenotype does not arise from an enhanced p53 response. In sensitive organs mitochondrial p53 accumulation in vivo occurs soon after a death stimulus. In subjects over 50, p53 Arg/Arg genotype is associated with increased risk of cutaneous melanoma as compared to genotypes Arg/Pro or Pro/Pro. In tumor cells lacking functional p53 and/or p21, p14(ARF) impaired mitotic entry and enforced a primarily cytoplasmic localization of p34(cdc2) that was associated with a decrease in p34(cdc2) kinase activity and reduced p34(cdc2) protein expression. Inactivation of p53 in osteosarcomas directly by mutation versus indirectly by HDM2 amplification may have different cellular consequences with respect to the stability of the genome. Inactivation of p53 is a protective mechanism utilized by cells to adapt to ER stress. Inactivation of p53 is an important cause of aberrant accumulation of beta-catenin in cancer cells. Increase in intracellular reactive oxygen species (ROS) associated with the magnitude of p53 protein expression correlated with the induction of either senescence or apoptosis in both normal and cancer cells. Increased expression is not an indicator of the presence of p53 gene mutations at exons 4-8 in hepatocellular carcinoma. Increased p53 and Ki-67 expression in varying grades of urothelial dysplasia of bladder. Inhibition by TP53 of G2 phase checkpoint abrogation and radiosensitization induced by PD0166285. Inhibition in HTLV-1-transformed cells is regulated by activated AKT. Inhibition of transcriptional activity was caused by E1B-AP5. Initiation of DNA replication is regulated by p53 through Cdc6 protein stability. Insulin inhibits TNF-alpha-dependent cell killing, induction of p53, p21 and apoptosis in a human cervical carcinoma cell line. Interaction of Ubc9 with p53 was regulated by phosphorylation of p53. Interactions with DNA in solution using time lapse atomic force microscopy. Inverse relationship seen between HPV infection and p53 positivity suggests loss of p53 function in cervical cancer, either by binding to E6 oncoprotein of HPV or by mutation in p53. Investigated whether Tat might alter p53 acetylation and p53-responsive transcription; results allude to mechanism where the HIV-1 trans-activator might impair tumor suppressor functions favoring establishment of neoplasia in AIDS. L structure of the p53 binding domain of USP7 alone and bound to an EBNA1 peptide. Levels of p53 are increased in three important brain tissues, i.e. frontal, parietal, and cerebellar cortices of autistic subjects, alluding to impaired apoptotic mechanisms in autism. Low incidence for actinic damage, basal cell and squamous cell carcinoma as documented in vitiligo could well reside in a protective function of up-regulated wild-type p53. Low-dose radiation hypersensitivity is associated with p53-dependent apoptosis. Maspin tumor suppressor expression is induced by p53 or TAp63gamma. Mechanism by which p68 may act as a tumour cosuppressor in governing p53 transcriptional activity. Mechanism of p53 regulation originating through alternative splicing of the human p53 gene resulting in the expression of a novel p53 mRNA. Mechanisms other than p53 may play a role in the regulation of bcl-2 expression in endometrial carcinoma. Mediation of apoptotic response in colorectal cancer cells by PUMA. Minor role of exon 5-9 among Sudanese breast cancer patients. Modulation of level by cyclin G via a negative feedback reglation. Molecular interactions of p53 within the N-terminal domain are not required to restrain DNA recombination, but might contribute to the genome stabilizing function. MtCLIC/CLIC4, an organellular chloride channel protein, is increased by DNA damage and participates in the apoptotic response to p53. Mutant MYC proteins, by selectively disabling a p53-independent pathway, enable tumour cells to evade p53 action during lymphomagenesis. Mutant p53 is reactivated and apoptosis is induced by maleimide analogs in human tumor cells. Mutant p53s are likely to be distinct in terms of the extent to which each mechanism contributes to their gain-of-function phenotypes. Mutants of p53 may induce loss of drug sensitivity is via the NF-kappaB2 pathway. Mutated p53 has a role in human papillomavirus type 38-positive non-melanoma skin cancers. Mutation analysis of this gene in a case of familial endometriosis. Mutations in TP53 do not have a role in formation of human cerebral vascular malformations. Mutations in epithelial ovarian cancer. Mutations in p53 gene can lead to enhanced chemoresistance; p53 gene may serve as a marker for NSCLC response to chemotherapy. Mutations in rheumatoid arthritis synovium. Mutations induce loss of DNA methylation and amplification of the TROP1 gene. New roles for several DNA damage response factors by demonstrating that they also participate in the oncogenic stress signaling pathway between E2F1 and p53. Nonagenarians and centenarians in good health have a statistically significant difference in the frequency of the GSTT1 deletion and the p53 genotypes when compared to younger controls; possible mechanisms for protection against aging are offered. Not very likely that TP53 mutations are involved in the etiology of meningiomas. Nuclear mutant p53 protein is expressed in early precancerous stages suggesting this is an early change in NSCLC tumorigenesis; may be a potential marker for development of NSCLC. Observations identify hMutL proteins as regulators of p53 response and demonstrate for the first time a function of hMLH1-hPMS1 complex in controlling the DNA damage response. Overexpression may be marker of radioresistance in head and neck cancer. Overexpression of p53 protein is observed in recurrent respiratory papillomatosis. Overproduction of Mdm2, resulting from a naturally occurring SNP, inhibits chromatin-bound p53 from activating the transcription of its target genes. P16INK4A, p14ARF, p53, and PCNA have roles in the progression of cervical neoplasia. P21 is highly correlated with p73 expression irrespective of the p53 mutation status in human esophageal cancers. P21WAF expression is induced by 5-Aza-CdR by demethylation of p73 leading to p53-independent apoptosis in myeloid leukemia. P29ING4 and p28ING5 may be significant modulators of p53 function. P35 reprter assays could not be ascribed to common dpible strand break-causing artifacts in standard genotoxicity screening. P53 accumulation and loss of bax expression influence the acquisition of a malignant phenotype but seem to have no further impact on tumor progression. P53 activates ATF3 in human tumor cells. P53 activation is inhibited by MDMX, which is transported to the cell nucleus with or without p53 upon DNA damage. P53 activation is not necessary for up-regulation of NOXA in melanoma cells. P53 activity and PIG3 gene function are uncoupled by UV-dependent alternative splicing through rapid proteolytic degradation. P53 activity is regulated by 14-3-3 sigma. P53 acts upstream of Bax to promote antineoplastics mediated cell death in a proline-rich domain-dependent manner through both transcription-dependent and -independent mechanisms in human colon cancer HCT116 cells. P53 alteration is an independent and significant indicator to predict unfavorable prognosis in patients with unresectable non-small cell lung cancer. P53 alterations commence as early as at the stage of benign and dysplastic nevi but there is no concordance between the frequent p53 protein expression and the rarity of both TP53 gene mutations in melanomas. P53 and c-Myc expression may have a role in regulation of telomerase activity in ovarian tumours. P53 and c-fos are significantly overexpressed in thyroid cancer patients, indicating their role in the genetic mechanisms leading to thyroid tumorigenesis. P53 and p21 act in series in mediating cell cycle arrest. However, the two risk factors, p53 proline homozygosity and p21 arginine allele, although part of a common causal pathway, appear to act in a mutually exclusive manner. P53 and p73alpha have roles in cell migration. P53 and recombination intermediates: role of tetramerization at DNA junctions in complex formation and exonucleolytic degradation. P53 antagonizes c-Myb by recruiting mSin3A to down-regulate specific Myb target genes. P53 as a sensor of transcriptional integrity. P53 basal transcription is regulated by down-regulation of protein kinase Cdelta. P53 binds telomeric single strand overhangs and t-loop junctions in vitro. P53 can directly induce Ipaf gene transcription, which contributes to p53-dependent apoptosis in at least some human cells. P53 causes brain tumor regression by suppressing tumor proliferation and indirectly induces involution of tumor vessels by fostering unopposed activity of Ang-2 in an environment of diminishing VEGF. P53 codon 72 genotype does not influence CIN risk in the Taiwanese population. P53 codon 72 polymorphism contributes to a genetically determined variability in apoptotic susceptibility among old people and may have a role in myocardial ischaemia. P53 codon 72 polymorphism may contribute to gastric cancer susceptibility. P53 contributes to the reversible, growth factor-dependent arrest of quiescence. P53 controls global nucleotide excision repair of low levels of structurally diverse benzo(g)chrysene-DNA adducts in human fibroblasts. P53 disruption has a dramatic effect on how glioblastoma cells process topoisomerase I inhibitor-mediated DNA damage. P53 does not have a role in 14-3-3sigma/IGF-I receptor mediation of cell cycle progression. P53 exhibited no statistical correlation with survival and disease-free survival. P53 expression and vascular density in colon cancer. P53 expression in HBV or HCV cirrhotic liver are a rather late event in carcinogenesis and related to hepatocellular carcinoma grade. P53 expression may have a role in progression of inflammatory breast cancer. P53 expression was an independent parameter related to a poor prognosis in diffuse large B cell non-Hodgkin's lymphomas. P53 function was lost by TP53 germline mutation with the loss of a wild type allele induced by the chemotherapy against ovarian cancer, leading to the development of MDS. P53 gen mutation analysis may be useful in the follow-up of at-risk patients, and introduces new possibilities to analyse molecular markers before malignant lesions are clinically apparent. P53 gene mutation is an independent predictor of poor prognosis in colorectal cancers. P53 gene mutation may be an early event in esophageal carcinogenesis. P53 gene mutations might be a main causal factor for carcinogenesis for gynecological neoplasms. P53 has a differential role in effecting G(2) arrest in response to topoisomerase II inhibitors, depending upon the mechanisms of action of the inhibitors tested. P53 has a pivotal role in apoptosis in the erythroid lineage development. P53 has a role in T-cell protein tyrosine phosphatase-induced apoptosis in a human tumor cell line. P53 has a role in cyclin D1-induced death signalling and causes caspase activation controlled by Bcl-2. P53 has a role in transactivation of the Fas gene during radiation-induced Fas sensitization in prostate cancer cells. P53 has different modes of high affinity DNA binding which are related to its tumor suppressor functions. P53 inactivation caused by HPV infection may play a role in the pathogenesis of colon cancer. P53 induced apoptosis is inhibited by Bcl-xL in head and neck neoplasms. P53 induced by ionizing radiation requires IFI16. P53 induces NF-kappaB activation by an IkappaB kinase-independent mechanism involving phosphorylation of p65 by ribosomal S6 kinase 1. P53 induces a faster mobilization of Axin into the degradation complex thereby enhancing beta-catenin turnover as part of a protective mechanism against the development of cancer. P53 induction and activation of DDR1 kinase counteract p53-mediated apoptosis and influence p53 regulation through a positive feedback loop. P53 inhibits transcriptional activation of invasion gene thromboxane synthase mediated by the proto-oncogenic factor ets-1. P53 interacts with RNA via its C-terminal domain; oligomerization of p53 is significantly enhanced by disrupting this. Binding of RNA to p53 is involved in the mechanism of p53 latency. P53 interacts with hRAD51 and hRAD54, and directly modulates homologous recombination. P53 is acetylated by tumor necrosis factor alpha, then p53 attenuates its trans-activation by depleting CREB binding protein in rheumatoid synoviocytes. P53 is an effective repressor of snRNA gene transcription by RNA polymerases II and III. P53 is an essential effector of PKCdelta in human colon cancer cells. P53 is an important mediators of chemoresistance in ovarian cancer cells. P53 is associated with the telomeric complex in alternative lengthening of telomeres (ALT) cells; inhibition of DNA synthesis in ALT cells by p53 requires intact specific DNA binding and suppression of recombination functions. P53 is inactivated by leukemic protein MLL-ELL. P53 is induced by urokinase in lung epithelial cells. P53 is involved in the progression of anal cancer and its expression increases from early in the development of pre-invasive anal lesions. P53 is not required for LKB1-induced apoptosis in pancreatic neoplasms. P53 is part of the survival pathway induced by integrin alpha4beta1 ligation and has a role in B-cell chronic lymphocytic leukemia drug resistance. P53 is recruited into the PML nuclear bodies by PML along with chk2. P53 is regulated by Kruppel-like factor 4 during G1/S cell cycle arrest in response to DNA damage. P53 is regulated by hGTSE-1 during apoptosis control after DNA damage in S and G2 phases. P53 is required for sensitization to TRAIL. P53 isoforms can regulate p53 transcriptional activity. P53 may exert transcriptional upregulation effects on c-FLIP gene and more potent effects on promoting the degradation of c-FLIP protein. P53 may have important roles in the regulation of cytokinesis through controlling the transcription of PRC1. P53 may play important role in transition from intraductal papillary-mucinous tumor of the pancreas adenoma to carcinoma in situ. P53 mediates DNA damaging drug-induced apoptosis by increasing its levels in the nucleus, thus inducing its transcription targets p21(Waf1/Cip1) and MDM2. P53 might be involved in homologous recombination and/or checkpoint function by directly binding to DMC1 protein to repress genomic instability in meiotic germ cells. P53 might play a protective role against cell damage induced by generation of intracellular ROS, through transcriptional activation of ALDH4. P53 must be dephosphorylated on serine residues during N-alpha-tosyl-L-phenylalanyl chloromethyl ketone-induced apoptosis. P53 mutants mediate the AI growth of LNCaP cells in an AR-independent fashion, and that both Akt and Bcl-2 are not involved in this process. P53 mutants showed increased binding to NQO1, which can explain their resistance to dicoumarol-induced degradation, as NQO1 has an important role in stabilizing hot-spot p53 mutant proteins in cancer. P53 mutation [p53(R273H)], is frequently found in human cancers. P53 mutation was found in 28% of sporadic adenocarcinomas respectively and in 0% and 22% of the 9 HNPCC cases. P53 mutational pathway may favor selection for ErbB2 gene amplification during tumor progression in breast cancer. P53 mutations and/or protein overexpression are a predictor of reduced postoperative survival after surgical resection of esophageal adenocarcinomas. p53 may be a clinically useful molecular marker for stratifying patients in clinical trials. P53 mutations are a later event in vulvar carcinoma. P53 mutations are an infrequent event in nasopharyngeal carcinoma in Spanish patients. P53 mutations are common among oral cavity cancers in the Brazilian population. P53 mutations in exon 7 might be associated with increased radiosensitivity in certain SCLC & NSCLC human lung cancer cell lines. No correlation concerning mutations in separate exons & response towards different chemotherapeutic agents could be found. P53 mutations reflected histological progression in Barrett's patients with p53 mutations found in 30% of metaplasia patients (P=0.4) and low-grade dysplasia patients (P=0.33). P53 mutations were found in 70% of pancreatic adenocarcinoma cell lines and 33% of primary tumors. p53 missense mutations correlated with more frequenct metastases to all sites. P53 mutations, in stromal cells can increase stromal-derived support of leukemia growth. Increased synthesis of pro-angiogenic cytokines, such as VEGF, may constitute one possible pathway by which this process is mediated. P53 negatively regulates intestinal immunity by delaying mucosal T cell cycling. P53 not only can provide proapoptotic signals but also regulates a survival pathway influencing Mcl-1 and Bcl-x(L) levels. P53 participates in a feedback mechanism with JNK to regulate the apoptotic process and is oppositely regulated by JNK1 and JNK2. P53 pathway mediates in part growth suppression by NaB and the p53 status may be an important determinant of chemosensitivity in HDI based cancer chemotherapy. P53 phosphorylation on six major serine sites is not required for activation of p53 target genes or biological responses in vivo. P53 plays a key role in luteinization of the primate ovarian follicle though the regulation of steroidogenic enzymes leading to progesterone synthesis. P53 plays an important role in PP2C alpha-directed cell cycle arrest and apoptosis. P53 polymorphism at codon 72 predicts the susceptibility to leiomyoma in a Caucasian population and may contribute to the pathogenesis of uterine leiomyoma. P53 positivity has been found only in part of the HGD cases and moreover a number of HGD with low or absent p53 scores has been found associated with high proliferation indices independently of the clinical evolution. P53 post-translational modification has a role in p53 inactivation in malignant epithelial cells with mdm2 gene amplification. P53 proteasomal degradation is regulated by NADPH quinone oxidoreductase 1 and independent of MDM2 and ubiquitin. P53 protein can directly induce permeabilization of the outer mitochondrial membrane by forming complexes with the protective BclXL and Bcl2 proteins, resulting in cytochrome c release. P53 protein expression is closely associated with decidual transformation indicates a novel role for this tumor suppressor in regulating human endometrial function. P53 protein increases in both neurons non-neuronal cells, including microglia, in HIV dementia. There may be a a novel role for p53 in the microglial response to gp120. P53 protein overexpression was noted in 59% of T-cell ltymphoblastic lymphoma cases and was correlaed with higher rate of relapse. P53 protein transport in hepatoma cells with VP22. P53 protein was analyzed in ovarian tumor samples and p53 exons were analyzed using SSCP and immunohistochemistry. 52% of tumors stained positive for p53; there was no correlation with telomerase activity based on p53 staining. P53 protein was estimated by immunohistochemistry of beta-catenin and p53 proteins in colorecta mucinous carcinoma. P53 represses TauT and is involved in renal development and apoptosis. P53 represses cyclin D1 transcription through down regulation of Bcl-3 and inducing increased association of the p52 NF-kappaB subunit with histone deacetylase 1. P53 represses myelocytomatosis oncogene c-myc transcription through a mechanism that involves histone deacetylation. P53 status is an important modulator of nitric oxide-induced mutagenesis and apoptosis, and suggest that level of the Apaf-1 ans XIAP proteins are regulated by p53. P53 was detected more frequently in CIN I compared with CIN II/III and invasive carcinoma. P53 was slightly increased in inverted follicular keratoses compared with inflammed or non-inflamed seborrheic keratoses. P53, Bax, Bcl-2 and Mdm2 mRNA expression levels correlate with the malignant transformation of the uterine cervix. P53, activated by NF-kappa B, is essential for H(2)O(2)-induced apoptosis in glioma cells. P53, bcl-2 and telomerase have roles in progression of Egyptian breast cancer patients. P53-dependent BRCA1 nuclear export is induced by DNA damage. P53-dependent apoptosis requires BOK and NOXA. P53-dependent apoptosis triggered by fast neutrons in lymphoid cells requires caspase 8-mediated BID cleavage. P53-dependent cell fate is determined by E1A-binding p300 nucleoprotein. P53-dependent loss of Fbxw7 leads to genetic instability by mechanisms that might involve the activation of Aurora-A, providing a rationale for the early occurrence of these mutations in human cancers. P53-induced apoptosis does not occur through the induction of CD95/CD95L expression. P53-induced apoptosis inhibited by activated Notch1. P53-induced apoptosis may be important for efficient cell lysis and viral spread and that E1B-19K may neutralize the apoptotic activity of p53 at multiple levels. P53-induced apoptosis was investigated through quantitative proteomic profiling using comparative amino acid-coded tagging. P53-induced transcription is inhibited by SINK-homologous serine-threonine kinase. P53-mdm2 binding is subtler than previously thought and involves global contacts such as multiple ""non-contiguous"" minimally structured motifs instead of being localized to one small helix mini-domain in p53 TAD. P53-specific serum antibodies are not associated with a history of skin carcinoma in renal transplant recipients and immunocompetent individuals. P53mt249 stimulates IGF-II dependent IGF-IR signaling by upregulating the expression of both ligand (IGF-II) and receptor (IGF-IR) through an autocrine and/or paracrine loop. P63 and p53 play a major role in the carcinogenesis of human esophageal squamous cells and in the growth of the carcinoma. P73, through HDM2, can oppose p53 tumor suppressor function and possibly contribute to tumorigenesis. PH-sensitive molecular defect of p53 (R337H)suggests that pH-dependent p53 dysfunction is the molecular basis for cases of adrenocortical carcinoma in Brazilian children. PRB degradation involved in gastric tumor cell apoptosis is p53-independent. Pathogenesis of nasopharyngeal carcinoma in children may involve EBV infection leading to LMP-1 expression and p53 overexpression. Persistence of induced levels of ROS in normal diploid human cells for 1 month after X-ray exposure and the role of TP53 in this oxidant response. Phosphorylation at multiple sites by ATM in response to ionizing radiation. Phosphorylation of p53 at Ser-215 by Aurora-A is a major mechanism to inactivate p53. Phosphorylation of p53 was rapidly induced in human fibroblasts upon exposure of cells to hydrogen peroxide (H(2)O(2)). Pivotal role of NO in the induction of cellular stress and the activation of a p53 response pathway during chronic inflammation. Placental transforming growth factor-beta as an important downstream mediator of DNA damage signaling and a transcriptional target of p53 (PTGF-beta). Polymorphism in codon 72 and risk of head and neck neoplasms. Possible interplay between p53 C-terminal phosphorylation and acetylation, and they provide an additional mechanism for the control of the activity of p53 by Checkpoint kinase 1 and Checkpoint kinase 2. Potential improvement of the International Prognostic Scoring System by the addition of molecular analysis to the system, with particular reference to the configuration of the TP53 gene. Proline-directed acetylation of p53 is a post-DNA binding event. Protection of p53 from MDM2 by PTEN and the damage-induced activation of PTEN by phosphorylated p53 leads to the formation of an apoptotic amplification cycle in which p53 and PTEN coordinately increase cellular apoptosis. Protein inhibitor of activated Stat1 (PIAS1) interacts with the tetramerization and C-terminal regulatory domains of p53 in yeast two-hybrid analyses. Protein kinase Calpha transcriptional repression via Sp1 by wild type p53 is involved in inhibition of multidrug resistance 1 P-glycoprotein phosphorylation. Protein stability measured by hydrogen exchange. Proximal 5'-flanking region of the IKKalpha gene contains a functional promoter reciprocally regulated by p53 and ETS-1. Reacts with glycogen synthase kinase-3beta after DNA damage. Recombinant p53 binds to BLM and WRN helicases and attenuates their ability to unwind synthetic Holliday junctions in vitro. Regulation of function by Pin1 during DNA damage. Repression of hTERT by endogenous p53 is mediated by p21 and E2F. Repression of p53 expression by signal transducer and activator of transcription 3 is likely to have an important role in development of tumors. Results demonstrated significant positive staining of p53 in the salivary tumorigenic tissue but not in the surrounding non-tumorigenic tissue, pointing to a biological role in the tumorigenic process. Results establish a direct functional link between p53 and human Rad51, and reveal that one of p53's functions in genome stabilization may be to prevent detrimental genome rearrangements promoted by Rad51. Results indicate HPV 16E6 may have multiple modes of interaction with E6AP and that assembly of p53 containing complexes for targeted degradation by E6AP may occur in more than one way. Results provide a novel mechanism, by which p53 is stabilized in tumor cells, and they suggest that a mediator should exist between ubiquitinated p53 and proteasome, which may be defective in H1299 cells. Results show that low levels of Mdm2 activity induce monoubiquitination and nuclear export of p53, whereas high levels promote p53's polyubiquitination and nuclear degradation. Results suggest that SAP contributes to the execution of some p53 functions. Results suggest that VEGF expression is involved in the promotion of angiogenesis in cervical neoplasia and that p53 is likely to be involved in the regulation of VEGF expression. Results suggest that microsatellite instability and p53 mutations are involved in tumor progression of dermatofibrosarcoma protuberans to fibrosarcoma as early and late events, respectively. Review of current knowledge about association of aneuploidy and p53. Review of the evidence for p53 as a participant in the responses of multiple CNS cell types to the presence of HIV and propose the hypothesis that HIV induced alterations in the CNS extracellular milieu converge at neuronal p53 activation. Review on mutations in brain neoplasms. Role for IGF-I in the regulation of the MDM2/p53/p21 signaling pathway during DNA damage. Role in adriamycin-induced senescence in breast tumor cells. Role in enhancing MUC2 mRNA expression. Role in inducing CD95 gene expression in endothelial cells exposed to doxorubicin. Role in inducing EGR1 contributes to enhanced transformed properties and resistance to apoptosis. Role in inducing cyclooxygenase 2 and in counteracting mutagen-induced apoptosis. Role in inhibiting p63 activity. Role in mediating cell cycle arrest in Rb(-/-) Saos2 cells. Role in mediating upregulation of CD95 gene expression upon genotoxic treatment in human breast tumor cells. Role in regulating expression of 67-kDa laminin receptor precursor 37LRP. Role in regulating growth-promoting gene IEX-1. Role in regulating survivin 2B. Role in the regulation of ceramide biosynthesis. Role of Cul4A in the MDM2-mediated proteolysis of p53. Role of binding to mdm2 protein in p53 regulation. Role of gene in the complexity of the mechanisms of initiation and maintenance of DNA damage-induced G2-phase arrest and subsequent G1-phase arres. Role of glycogen synthase kinase-3beta in binding and promoting action of p53. Role of p53 as a major pro-apoptotic factor in the pathogenesis of AIDS [review]. Role of p53 gene in the biophysics and biology in murine erythroleukemia cell line with the goal of understanding the influence of this tumor suppressor gene on the deformability and metastasis of tumor cells. Role of pathway in regulating G1-S transition and apoptosis along with RFT. Role of tyrosine phosphorylation of Mdm2 by c-abl in p53 regulation. Search for the factors interacting with NTH1 shows GST-NTH1 fusion protein precipitates proliferating cell nuclear antigen (PCNA) and p53 as well as XPG from human cell-free extracts. Sequestration of replication protein A by p53 at the sites of recombination is one means by which p53 can inhibit homologous recombination processes. Show that the Bcl-x(L) interaction surface on p53 involves the same region that is used by the protein to contact DNA. The p53-binding site on Bcl-x(L) is also defined. Small airway epithelial cells expressing a p53 mutant alleles were able to inhibit endogenous p53 activity; only one allele, 248W demonstrated a markedly increased ability to facilitate E1B 55-kilodalton protein-deficient adenovirus (ONYX-015) replication. Solar UV rays in cause mutations in p53- specifically CC-->TT transitions- which lead to squamous cell carcinoma of the conjunctiva. Spindle cell component of this case was genetically characterized by loss of heterozygosity (LOH) at a codon 234 of exon 7 of the p53 gene. Studies define a novel p53-survivin signaling pathway activated by DNA damage that results in down-regulation of survivin, cell cycle arrest, and apoptosis. Study establishes poly(ADP-ribose) polymerase-1 as a critical regulator of the protein p53 response to DNA damage. Study showed that polymorphism at codon 72 of TP53 gene is not associated with an increased susceptibility to cervical disease and/or HPV infection in the Argentine women population. Summarize the current understanding of post-translational modifications and their effect on conformation-based functional relationship between Mdm2 and p53. Suppression of p53-C277Y by RNAi reduced pig3 promoter activity, RNA, and protein expression. Survivin can reduce the cell growth inhibition and apoptosis, and p53 elevates the p21 level, which may attenuate the cell death in the quercetin-treated human lung carcinoma cells. Survivin, p53, and bcl-2 are elevated in breast carcinoma but not ductal intraepithelial neoplasia. Sustained inactivation of the p53 pathway by the HPV16 E6 protein is required for maintenance of the proliferative phenotype of HeLa cervical carcinoma cells. Systematic automated analysis of the effects of p53 mutations on the structure of the core domain of the protein. That variations in TP53 and hCAD genes modulate the age of onset of Huntington disease. That wt-tumor protein p53 gene transfer inhibits interleukin 8 production and NF-kappaB transcription activity in cancer cells. The MDM2-L5-L11-L23 complex functions to inhibit MDM2-mediated p53 ubiquitination and thus activates p53. The N-terminal domain of PIAS1 interacts with DNA as well as p53. The data demonstrate that wild-type p53 in cytoplasm, in its noninduced state, is functional; it displays intrinsic 3'-->5' exonuclease activity. The expression of DAP kinase, p19ARF, p53, and p21WAF1 was significantly down-regulated in the chronically HIV-1SF2-infected HUT78 T cells. The expression of p53 is very probably involved in the regulation of leukemic hematopoiesis and that the inhibition of p53 expression could modulate the proliferation of leukemic cells. The greater severity of TP53-mutant B-CLLs compared with ATM-mutant B-CLLs is consistent with the additive effect of defective apoptotic and elevated survival responses after DNA damage in these tumors. The increased malignancy of cancer cells resulting from loss of p53 may be mediated, in part, through the choline phospholipid pathway. The inhibitory protein c-FLIP(L) is involved in resistance to CD95-mediated apoptosis in ovarian carcinoma cells with wild-type p53. The lack of correlation between p73 or p63 and p53 expression in head and neck squamous carcinoma suggests an independent and/or compensatory functional role. The net deubiquitination of the various targets of HAUSP determines the steady-state level of p53. The number of p53 gene alterations in low-grade central osteosarcomas is lower than that in conventional high-grade osteosarcomas. The p53 gene polymorphism may associate with NPC susceptibility in Thai population, particularly the Pro/Pro genotype carriers with age of >40 years. The p53 mutant p53R282del found in neuroblastoma cells is a non-functional mutant and has no dominant negative nature. The p53 tetramerization domain can be converted from the soluble native state to amyloid-like fibrils under certain conditions. The persistence of p53 overexpression after Bacillus Calmette-Guerin intravesical therapy is predictive of progression in patients treated for carcinoma in situ. The presence or absence of wild-type p53, may be an important determinant of response to antiangiogenic therapy. The promoter specificity plays an important role in selective activation of p53 DNA binding by c-Abl. There are high frequencies of somatic mutations in TP53 (encoding tumor protein p53) in breast neoplastic epithelium and stroma. There is a mitotic checkpoint wherein p53-dependent activation of Snk/Plk2 prevents mitotic catastrophe following spindle damage. There is a relationship between the p53 pathway and the ubiquitin-mediated degradation of mitotic cyclins and possible cross-talk between the G2-DNA damage checkpoint and the mitotic checkpoint. There may be a p53-dependent regulatory pathway of the maspin protein in human cancer. This gene regulates the matastasis suppressor gene Nm23 in cultured tumor cells. Thymidylate synthase and p53 have roles in regulating Fas-mediated apoptosis in response to antimetabolites. Tp53 has a role in apoptosis along with noxa protein in human tumor cells. Tp53 has a role in recruitment of nucleotide excision repair factors XPC and TFIIH to DNA damage. Tp53 may negatively control the MAKP pathway via MKP1. Transcription of the p53 gene is induced by IFN-alpha/beta, accompanied by an increase in p53 protein level, contributing to tumour suppression and critical for antiviral defence. Trp53 has a role in activation of the Fas/CD95 pathway. Tumour-suppressor protein p53 is a COP1-interacting protein; COP1 is a critical negative regulator of p53. Two sequence motifs from HIF-1alpha bind to the DNA-binding site of p53. Types of mutations in sinonasal NK/T cell lymphoma in northeast district of China. Ultraviolet rays increase the specificity of CK2 for p53 at the expense of other cellular CK2 substrates and leading to an overall increase in p53 serine 392 phosphorylation. Uncoupling of the electrochemical gradient by increased manganese superoxide dismutase activity gives rise to p53 up-regulation. Unique mechanism for p53 regulation by the p65/RelA subunit of NF-kappaB. Upon activation by DNA damage, wt p53 mediates an accelerated degradation of HIF-1alpha protein, resulting in reduced activation of CA9 transcription and, correspondingly, decreased levels of CAIX protein. Use of p53MH algorithm in detection of p53-responsive genes. V-Fos-stimulated invasion is independent of the pRb/p16(INK4a) and p53 tumor suppressor pathways and telomerase. Value of this tumor marker regarding relapse, metastasis and death in resectable non-small cell lung cancer. Were not able to confirm that the TP53 polymorphism at exon 4 increases the susceptibility to be infected by HPV or to develop high-grade intra-epithelial lesion of the cervix. When p53 protein levels increase, it contributes to its own demise by up-regulating the transcription of S100B protein as part of a negative feedback loop. X-ray crystallography of mutant human p53 core domain.
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